OBM Genetics is an international Open Access journal published quarterly online by LIDSEN Publishing Inc. It accepts papers addressing basic and medical aspects of genetics and epigenetics and also ethical, legal and social issues. Coverage includes clinical, developmental, diagnostic, evolutionary, genomic, mitochondrial, molecular, oncological, population and reproductive aspects. It publishes a variety of article types (Original Research, Review, Communication, Opinion, Comment, Conference Report, Technical Note, Book Review, etc.). There is no restriction on the length of the papers and we encourage scientists to publish their results in as much detail as possible.

Publication Speed (median values for papers published in 2023): Submission to First Decision: 5.1 weeks; Submission to Acceptance: 17.0 weeks; Acceptance to Publication: 7 days (1-2 days of FREE language polishing included)

Current Issue: 2024  Archive: 2023 2022 2021 2020 2019 2018 2017
Open Access Review

MiRNAs as Promising Therapeutic Targets for Breast Cancer

Morkoss M. Fakhry 1, Asmaa R. Abdel-Hamed 2, Noha M. Mesbah 2,*, Dina M. Abo-Elmatty 2, Mohamed M. Sayed-Ahmed 3, Abdel-Moneim M. Osman 3, Ola S. Ahmed 4

  1. Biochemistry Department, Faculty of Pharmacy, Egyptian Russian University, Cairo, Egypt

  2. Department of Biochemistry, Faculty of Pharmacy, Suez Canal University, Ismailia, Egypt

  3. Pharmacology and experimental oncology Unit

  4. Virology and Immunology Unit, National cancer institute, Cairo University, Cairo, Egypt

Correspondence: Noha M. Mesbah

Academic Editor: Lunawati L Bennett

Received: November 27, 2023 | Accepted: February 18, 2024 | Published: February 26, 2024

OBM Genetics 2024, Volume 8, Issue 1, doi:10.21926/obm.genet.2401215

Recommended citation: Fakhry MM, Abdel-Hamed AR, Mesbah NM, Abo-Elmatty DM, Sayed-Ahmed MM, Osman AM, Ahmed OS. MiRNAs as Promising Therapeutic Targets for Breast Cancer. OBM Genetics 2024; 8(1): 215; doi:10.21926/obm.genet.2401215.

© 2024 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.


Breast cancer (BC) is the most common cause of cancer-related death and is the malignancy most frequently diagnosed in females worldwide. BC incidence is predicted to continue increasing worldwide. Without interventions, annual new cases will reach over 3 million by 2030. Genetic abnormalities account for almost 70% of all BC cases worldwide. Biological pathways implicated include non-coding RNAs (ncRNAs). MiRNAs are small non-coding RNA molecules that play a role in post-transcriptional regulation of gene expression. They can function as either tumor suppressors or oncogenes, and their role depends on the specific miRNA and target genes affected. The research on miRNA-based cancer treatments has yielded promising results. Depending on recent data, the goal of this review was to summarize the mechanisms that explain the role of some miRNAs in BC pathogenesis and drug resistance. However, highlighting the areas needing further exploration and more research is required before using microRNAs in clinical settings.


miRNA; clinical; cancer; drug resistance; breast; pathways; death

1. Introduction

Cancer is characterized by uncontrollable cell growth and invading other body tissues. Malignant tumors are another name for cancerous tumors. Benign tumors do not spread or invade near tissues. In the case of benign tumor removal, they rarely reoccur, whereas cancerous tumors do on occasion. Benign tumors can grow to be quite large at times, but some can cause severe symptoms or be fatal, such as benign tumors in the brain [1,2].

Breast cancer (BC) is known as a type of cancer that starts in the breast. It starts in one or both breasts and occurs almost entirely in women, but men can get BC, too. Breast cancers can develop in many locations within the breast [3]. Breast cancer remains the most commonly diagnosed cancer in women worldwide. In 2020, an estimated 2.3 million new cases of BC were diagnosed globally [4,5]. Younger women are being diagnosed at increasing rates, potentially attributed to factors such as obesity, alcohol consumption, and reproductive patterns [6,7]. In the present time, many therapeutic regimens for BC were developed can be enumerated as the following:

  • Surgery, which is the primary treatment for localized BC, is the surgical removal of the tumor via lumpectomy or mastectomy. It aims to remove all cancer from the breast and nearby lymph nodes [8,9].
  • Chemotherapy is used to treat many types of BC, especially when cancer has spread. Common chemodrugs include anthracyclines, taxanes, 5-FU, and cyclophosphamide, which are given before or after surgery [10,11].
  • Radiation therapy is given after lumpectomy to destroy any remaining cancer cells and reduce the risk of recurrence. External beam radiation is directed at the breast or chest wall [12,13].
  • Hormonal therapy is used for hormonally-responsive cancers like ER+ or PR+, for example, tamoxifen and aromatase inhibitors (e.g., anastrozole, letrozole, exemestane). Given for 5-10 years after initial treatment [14].
  • Targeted therapy that targets specific molecules involved in cancer growth. Examples are trastuzumab for HER2+ cancer, palbociclib, and ribociclib for ER+/HER2- metastatic disease [15].
  • Immunotherapy is a treatment approach that uses drugs, such as atezolizumab and pembrolizumab, to help the immune system better recognize and destroy cancer cells [16,17].
  • Combination therapy uses multi-modality treatment involving a combination of the above approaches depending on cancer stage, grade, and receptor status. The goal is to achieve the highest possible effectiveness in treatment while keeping the side effects within acceptable limits [18].

Our understanding of the biological regulation of genetic material has advanced significantly over the last two decades. The genome has 2% protein-coding genes and more than 90% non-coding protein genes. Protein-coding genes undergo translation into proteins following transcription to RNA. Non-coding protein genes are transcribed but not translated into proteins [19]. Non-coding RNA is essential for genetic regulation. miRNAs are non-coding RNAs that are crucial in numerous diseases [20].

MicroRNA, regarded as a non-coding RNA, was discovered in 1993 in the nematode Caenorhabditis elegans. It is a member of the endogenous small non-coding RNA family. It is composed of ~22 nucleotides [21]. They participate in the posttranscriptional regulation of gene expression through one of two mechanisms: mRNA translation suppression or mRNA degradation. miRNA target sites are found in the 3'-UTR of more than 60% of human protein-coding genes. As a result, those genes are regulated by miRNA [22]. According to the miRNA database, over 1000 miRNAs have been identified in the human genome. Those miRNAs regulate 1 to 5% of human gene expression. As a result, miRNAs are one of the most numerous classes of genomic regulators [23].

One of the earliest studies discussing the relation of miRNAs and breast cancer is the work by Costinean, Sandhu, and colleagues from the Croce lab, who reported the first in vivo evidence implicating the overexpression of a miRNA in cancer. They found that miR-155 directly caused a leukemic phenotype. The following year, the Slack group reported that a single oncogenic miRNA, miR-21, was enough to cause neoplastic development in a mouse model with no predisposing mutations. These findings suggested that tumors could become addicted to miR-21, similar to the phenomenon of addiction to oncogenic proteins [24,25,26].

In a review by Lu et al. (2005), the authors reported the differential expression of miRNAs in breast cancer. They demonstrated that miRNAs could perform their function as oncogenes or tumor suppressors. They also discussed the potential of miRNAs as diagnostic and prognostic markers in BC therapy [27,28]. So, in this review article, we will discuss some miRNAs' role in BC pathogenesis.

2. The Biogenic Pathway of miRNAs

Two main pathways exist for generating miRNAs from genetic sequences in the genome (see Figure 1).

Click to view original image

Figure 1 Biogenic pathways of miRNAs.

2.1 Canonical/non conical Pathways of miRNA Biogenesis

miRNA genes are transcribed by RNA polymerase II into long primary miRNA transcripts (pri-miRNAs) that can be several kilobases long. In the nucleus, the pri-miRNA is cleaved by the Drosha RNase complex into a 60-70 nucleotide stem-loop precursor miRNA (pre-miRNA). The pre-miRNA is then exported from the nucleus into the cytoplasm by Exportin-5. Dicer cleaves off the loop in the cytoplasm, leaving a short double-stranded miRNA/miRNA* duplex around 22 nucleotides long. One strand of the duplex is associated with the RNA-induced silencing complex (RISC) to regulate target mRNAs [29,30].

2.2 Non-Canonical/Mirtrons Pathways

Some miRNAs are situated within the introns of genes that encode proteins. The splicing machinery spliced and debranched the intron, generating a pre-miRNA-like structure without the involvement of Drosh. This pre-miRNA is then exported and processed similarly by Dicer/RISC [31].

So, miRNAs predominantly undergo canonical nuclear processing by Drosha and Dicer, but a minor fraction uses the non-canonical mirtron pathway dependent on splicing alone. Both ultimately produce mature functional miRNAs incorporated into RISC.

3. Breast Cancer and Micro-RNAs

Because of their stability in blood and differential expression in different tissues and diseases (Table 1), miRNAs have received much attention as cancer biomarkers. There is also the option of repeating measurements in a non-invasive manner. The underlying miRNA's mechanisms of high stability in an RNAase-rich environment are still unidentified. Two hypotheses about how miRNAs in circulation protect themselves against degradation are reported. The first hypothesis proposes that miRNAs are found in apoptotic bodies, microvesicles, lipoproteins, lipids, or exosomes [32,33]. The second hypothesis proposes that miRNA is present in protein complexes. Almost all circulating miRNAs were recently discovered with protein complexes co-fractionated and bound to Argonaute proteins, indicating that they remain stable in circulation even when removed from the exosome [34,35].

Several studies have discovered differences in miRNA expression in BC patients versus healthy subjects in blood or tissue. They suggested they could be used as predictive, prognostic, or diagnostic biomarkers. miRNA profiling in circulation has been proposed as a novel technique for detecting BC in the early stages [36]. A pilot study proposed that changes in circulating miRNA concentrations (up-or-down-regulation) could be used as markers in early detection of BC [37]. Furthermore, some miRNAs, such as miR-21 overexpression, have been linked to an advanced stage of the tumor, lymph node metastasis, and poor survival [38]. Some miRNA expression levels, such as miR-375 and miR-9, were strongly associated with ER+ BC. Other miRNAs' expression levels changed after treatment [39,40,41]. A different type of cancer was found to have higher miR-21 expression levels. When comparing BC patients to healthy subjects, researchers discovered increased miR-21 expression in their serum. It was found to be more abundant in primary breast cancer tissues and breast cancer cell lines [42,43].

MicroRNA-375 (on chromosome 2q35) was discovered as a -cell regulator for function and development and insulin secretion in pancreatic islets by targeting the PDK-1 and MTPN genes [44]. According to additional research, miRNA-375 is involved in multiple types of cancer by targeting several important genes such as AEG-1, YAP1, and IGF1R [45]. miR-375 has been proposed to function as an oncogene or a tumor suppressor, depending on the specific gene targets in various cancer types. However, its role in BC remains a topic of debate [46].

miR-155 expression levels are consistently upregulated in breast tumor samples, acting as an anchor-miRNA. miR-155 has been linked to clinical markers, aggressive tumors, and decreased survival in BC patients. Some contradictory findings have been reported, such as the variable association of miR-155 with hormone receptor status [47]. It is also unclear whether miRNA-155 causes cancer or promotes its progression. miR-155 has been shown in a mouse model to transform B-cells, but only in breast cells has it been shown to enhance cancerous properties. More research is needed to fully comprehend the significance of elevated miR-155 levels in BC [48].

In BC xenograft models and cell lines, miRNA-155 promotes tumor growth and cell proliferation, inhibits apoptosis, and mediates TGF-driven EMT. Since miRNA-155 levels are elevated in invasive tumors and BC metastases, the role of miRNA-155 in EMT holds promising therapeutic potential [49]. Also, many miRNAs play regulatory roles in BC, which can be summarized by the following:

  • Control of cell proliferation: miRNAs regulate genes involved in cell cycle progression and replication. Deregulation contributes to the uncontrolled growth of cancer cells [50].
  • Regulation of apoptosis: Both pro- and anti-apoptotic genes are targeted by miRNAs, affecting susceptibility to programmed cell death. Misregulation promotes the survival of damaged cells [51].
  • Modulation of invasion and metastasis: miRNAs influence EMT, extracellular matrix degradation, angiogenesis, and other processes involved in cancer cell invasion and spread to other organs [52].
  • Metabolic reprogramming: Emerging role in regulating cancer cell metabolism at the post-transcriptional level to support bioenergetic and biosynthetic demands of rapid proliferation [53].
  • Stem cell regulation: miRNAs are implicated in the self-renewal and differentiation of normal and cancer stem cells, believed to drive tumor initiation and recurrence [54].
  • Treatment response: Aberrant miRNA levels modulate sensitivity to chemotherapy, radiotherapy, hormonal, and targeted agents. May influence the acquisition of resistant phenotypes [55].
  • Epigenetic and genetic regulation: Reciprocal regulatory interactions between miRNAs and other epigenetic/genetic factors form complex networks governing breast cancer pathogenesis [56].
  • Immune modulation: Impact anti-tumor immunity through local and systemic effects on immune cell populations, cytokine production, and immune checkpoints [57].
  • Tumor microenvironment: Crosstalk with stromal cells influences multiple processes like angiogenesis and tumor-promoting inflammation [58].

So, in summary, miRNAs control numerous facets of breast cancer biology at the post-transcriptional level. Their deregulation has wide-ranging impacts on disease behavior and outcomes.

4. The Dual Role of miRNAs in BC

MicroRNAs can act as oncogenes and tumor suppressors (Table 1) in BC development and progression. Their role depends on the specific miRNA and target genes affected. Oncogenic miRNAs, also known as oncomiRs, are frequently upregulated in BC. They promote tumor growth and metastasis by repressing tumor suppressor genes. Examples include the miR-17-92 cluster and miR-21, which target apoptosis, proliferation, and metastasis genes. Other miRNAs can function as oncogenes by negatively regulating the expression of tumor suppressor genes, and upregulation of these miRNAs inhibits anti-cancer genes, again promoting tumor growth and progression for examples, miR-21, miR-155, miR-10b, miR-373, and miR-520c [59,60,61].

Tumor suppressor miRNAs are commonly downregulated in BC, and their decrease contributes to uncontrolled cell growth. For instance, the miR-205/200 families typically suppress oncogenes such as RAS, HER2/neu, and ZEB1/2. Low levels of these miRNAs deactivate tumor suppressive pathways [62,63].

Depending on tumor stage and subtype, the same miRNA can function as both an oncogene and tumor suppressor. For example, high miR-10b promotes metastasis, but low levels also contribute to invasion and progression in some subtypes. The targets of a given miRNA and the cellular context determine whether it drives tumor initiation or suppresses cancer cells [64,65]. Overall, the precise regulatory roles of miRNAs are complex and context-dependent in BC development. Understanding their dual functions is important for developing new prognostic biomarkers and miRNA-based therapies Table 1.

Table 1 Changes in miRNA expression in BC. (According to previously reported data by other research groups).

5. MicroRNAs and BC Drug Resistance

MiRNAs play a critical role in medication resistance. Several miRNAs, including miR-451, miR-200c, miR-298, and miR-27a, have been found to affect doxorubicin in BC cell lines. Few studies, however, have found a link between drug resistance in patients and miRNAs. A recent study, for example, discovered that miR-200c was upregulated in chemoresistant patients' BC tissues compared to responders [110]. In contrast, other studies using breast cancer tissues found a link between low miR-200c expression and poor response to neoadjuvant chemotherapeutics [111]. In these cases, the exact mechanism underlying the drug resistance is unknown; however, some clues can be identified through cell line studies. Other pathways can influence drug resistance and, as a result, be miRNA targets. For example, down-regulation of miR-15a/16 causes an increase in the anti-apoptotic protein BCL2 and, as a result, tamoxifen resistance. This occurs due to oncogenic HER216's alternative regulation of the miR-15a/16 cluster, found in more than 30% of ER+ tumors [112,113]. As a result, this could explain some patients' poor treatment outcomes. MiR221/222 cluster, on the other hand, targets the cell cycle inhibitor p27Kip1 to act as an oncogenic miRNA. Tamoxifen resistance was linked to low levels of p27Kip1 [114]. Interestingly, The presence of the miR-221/222 cluster influences fulvestrant resistance, most likely by targeting the previously mentioned protein. MiR221/222 can act as a tumor suppressor and an oncogenic miRNA in this case [115,116].

MiR-221/222 levels rise in response to fulvestrant treatment, and it suppresses the growth of tumors by targeting the ER. On the other hand, long periods of estradiol deprivation can result in constitutively increased expression of miR-221/222, which becomes oncogenic by targeting cell cycle inhibitors like p27Kip1 [117,118].

MiR-128a is another hormone-responsive miRNA that is overexpressed in letrozole-resistant cell lines and can enhance cell growth and resistance to letrozole by targeting TGF. Inhibition of miR-128a restores TGF inhibition, leading to increased sensitivity of cells to letrozole. Because miR-128a is highly expressed in cells with high hormone levels [119]. In a drug-resistant cell line, MiR-125b is indeed upregulated. MiR-125b, in particular, is overexpressed in taxol-resistant cell lines, inhibiting taxol's apoptotic effect. Most likely, miR-125b causes this resistance by targeting BAK1, a pro-apoptotic protein [120,121]. Concurrent administration of a miR-21 inhibitor and taxol improved chemotherapeutic agent toxicity and, as a result, apoptosis in the MCF-7 cell line. This study shows that using miRNA inhibitors in some tumors is feasible. However, caution is advised, as is additional research into the potential side effects of using miRNAs/anti-miRNAs as a therapy [122,123]. Trastuzumab appears to be influenced by miR-21 in HER2/3 targeted therapy, whereas lapatinib and gefitinib appear to be influenced by miR-205 [124,125].

6. The Future Aspects Concerning Developing Therapeutic Targets of BC

The role of microRNAs (miRNAs) in developing therapeutic targets for breast cancer is expected to evolve, as these small non-coding RNAs play a crucial role in regulating gene expression at the post-transcriptional level. miRNAs are involved in the main biological behaviors of tumors, making them attractive targets for anticancer drug development [126,127,128]. Some key aspects of the future vision for miRNA-based therapeutics in breast cancer include:

6.1 Nanotechnology-Mediated Delivery

Nanoparticles (NPs) loaded with miRNAs have shown promise in precisely targeting and silencing oncogenic miRNAs, which could help improve the efficacy of cancer chemotherapy and mitigate its associated unwanted side effects [129,130].

6.2 Clinical Trials

Clinical trials examining the clinical potential of miRNAs as biomarkers for cancer therapy diagnosis and prognostication are underway, with some trials focusing on diagnostic miRNAs in blood or tissue samples from cancer patients [131].

6.3 Improved Drug Strategies

Ongoing clinical trials are exploring advanced delivery technologies and synthetic RNA molecules to enhance the efficacy of miRNA-based therapies [132,133].

6.4 Combination Therapies

miRNAs could be combined with other therapeutic agents, such as chemotherapy drugs, to enhance their effectiveness in treating BC [134,135].

Despite the progress made in miRNA-based therapeutics, there are still challenges to overcome, such as the limitations of current detection methods and the need for more efficient and cost-effective approaches. Overcoming these challenges could pave the way for miRNA detection and treatment to enter the clinic smoothly and become a new target for BC treatment [136,137].

7. Conclusion

MicroRNAs demonstrate a dual role in BC development and progression depending on the specific miRNA and context. Both increases and decreases in miRNA expression can promote breast tumorigenesis, so targeting specific oncogenic or tumor-suppressive miRNAs holds promise as a therapeutic strategy, either by inhibiting oncogenic miRNAs or restoring loss of tumor-suppressive miRNA function through supplementation.

List of Abbreviations

Author Contributions

Asmaa R. Abdel-Hamed participated in the design of the study, data curation and investigation and manuscript writing. Morkoss M. Fakhry was responsible for the laboratory work and writing the original draft and resources of the manuscript. Noha M. Mesbah and Dina M. Abo-Elmatty participated in the design of the study, drafting, and revising the work, and final approval of the submitted version. Mohamed M. Sayed-Ahmed, Abdel-Moneim M. Osman and Ola S. Ahmed participated in data analysis, drafting, and revising the work.

Competing Interests

The authors have declared that no competing interests exist.


  1. Yuan Z, Li Y, Zhang S, Wang X, Dou H, Yu X, et al. Extracellular matrix remodeling in tumor progression and immune escape: From mechanisms to treatments. Mol Cancer. 2023; 22: 48. [CrossRef]
  2. Brown JS, Amend SR, Austin RH, Gatenby RA, Hammarlund EU, Pienta KJ. Updating the definition of cancer. Mol Cancer Res. 2023; 21: 1142-1147. [CrossRef]
  3. Jesinger RA. Breast anatomy for the interventionalist. Tech Vasc Interv Radiol. 2014; 17: 3-9. [CrossRef]
  4. Kinnel B, Singh SK, Oprea-Ilies G, Singh R. Targeted therapy and mechanisms of drug resistance in breast cancer. Cancers. 2023; 15: 1320. [CrossRef]
  5. Zhao X, Richardson DR. The role of the NDRG1 in the pathogenesis and treatment of breast cancer. Biochim Biophys Acta Rev Cancer. 2023; 1878: 188871. [CrossRef]
  6. Fentie H, Ntenda PA, Tiruneh FN. Dietary pattern and other factors of breast cancer among women: A case control study in Northwest Ethiopia. BMC Cancer. 2023; 23: 1050. [CrossRef]
  7. Hirko KA, Lucas DR, Pathak DR, Hamilton AS, Post LM, Ihenacho U, et al. Lifetime alcohol consumption patterns and young-onset breast cancer by subtype among non-Hispanic black and white women in the young women’s health history study. Cancer Causes Control. 2023; 35: 377-391. [CrossRef]
  8. Khan SY, Cole J, Habrawi Z, Melkus MW, Layeequr Rahman R. Cryoablation allows the ultimate de-escalation of surgical therapy for select breast cancer patients. Ann Surg Oncol. 2023; 30: 8398-8403. [CrossRef]
  9. Ozmen T, Ozmen V. Treatment changes in breast cancer management and de-escalation of breast surgery. Eur J Breast Health. 2023; 19: 186-190. [CrossRef]
  10. Wimmer K, Sachet M, Ramos C, Frantal S, Birnleitner H, Brostjan C, et al. Differential immunomodulatory effects of epirubicin/cyclophosphamide and docetaxel in breast cancer patients. J Exp Clin Cancer Res. 2023; 42: 300. [CrossRef]
  11. Brianna, Lee SH. Chemotherapy: How to reduce its adverse effects while maintaining the potency? Med Oncol. 2023; 40: 88. [CrossRef]
  12. Hasan MM, Mohanan P, Bibi S, Babu C, Roy YJ, Mathews A, et al. Radiotherapy in breast cancer. Interdisciplinary cancer research. Cham: Springer; 2023. [CrossRef]
  13. Tran J, Thaper A, Lopetegui-Lia N, Ali A. Locoregional recurrence in triple negative breast cancer: Past, present, and future. Expert Rev Anticancer Ther. 2023; 23: 1085-1093. [CrossRef]
  14. Tagde P, Najda A, Nagpal K, Kulkarni GT, Shah M, Ullah O, et al. Nanomedicine-based delivery strategies for breast cancer treatment and management. Int J Mol Sci. 2022; 23: 2856. [CrossRef]
  15. Viganò L, Locatelli A, Ulisse A, Galbardi B, Dugo M, Tosi D, et al. Modulation of the estrogen/erbb2 receptors cross-talk by cdk4/6 inhibition triggers sustained senescence in estrogen receptor-and erbb2-positive breast cancer. Clin Cancer Res. 2022; 28: 2167-2179. [CrossRef]
  16. Liu Y, Hu Y, Xue J, Li J, Yi J, Bu J, et al. Advances in immunotherapy for triple-negative breast cancer. Mol Cancer. 2023; 22: 145. [CrossRef]
  17. Al-Taie A, Sheta N. Clinically approved monoclonal antibodies-based immunotherapy: Association with glycemic control and impact role of clinical pharmacist for cancer patient care. Clin Ther. 2023; 46: e29-e44. [CrossRef]
  18. Oertel M, Schlusemann T, Shumilov E, Reinartz G, Bremer A, Rehn S, et al. Radiotherapy in combination with systemic therapy for multiple myeloma-a critical toxicity evaluation in the modern treatment era. Cancers. 2023; 15: 2909. [CrossRef]
  19. Wang F, Scoville D, He XC, Mahe MM, Box A, Perry JM, et al. Isolation and characterization of intestinal stem cells based on surface marker combinations and colony-formation assay. Gastroenterology. 2013; 145: 383-395. [CrossRef]
  20. Devaux Y, Vausort M, Goretti E, Nazarov PV, Azuaje F, Gilson G, et al. Use of circulating microRNAs to diagnose acute myocardial infarction. Clin Chem. 2012; 58: 559-567. [CrossRef]
  21. Carberry CK, Koval LE, Payton A, Hartwell H, Kim YH, Smith GJ, et al. Wildfires and extracellular vesicles: Exosomal microRNAs as mediators of cross-tissue cardiopulmonary responses to biomass smoke. Environ Int. 2022; 167: 107419. [CrossRef]
  22. Singh RP, Massachi I, Manickavel S, Singh S, Rao NP, Hasan S, et al. The role of miRNA in inflammation and autoimmunity. Autoimmun Rev. 2013; 12: 1160-1165. [CrossRef]
  23. Palmero EI, de Campos SG, Campos M, Souza NC, Guerreiro ID, Carvalho AL, et al. Mechanisms and role of microRNA deregulation in cancer onset and progression. Genet Mol Biol. 2011; 34: 363-370. [CrossRef]
  24. Lee R, Feinbaum R, Ambros V. A short history of a short RNA. Cell. 2004; 116: S89-S92. [CrossRef]
  25. Orellana EA, Kasinski AL. MicroRNAs in cancer: A historical perspective on the path from discovery to therapy. Cancers. 2015; 7: 1388-1405. [CrossRef]
  26. He L, Hannon GJ. MicroRNAs: Small RNAs with a big role in gene regulation. Nat Rev Genet. 2004; 5: 522-531. [CrossRef]
  27. van Schooneveld E, Wildiers H, Vergote I, Vermeulen PB, Dirix LY, Van Laere SJ. Dysregulation of microRNAs in breast cancer and their potential role as prognostic and predictive biomarkers in patient management. Breast Cancer Res. 2015; 17: 21. [CrossRef]
  28. Bombonati A, Sgroi DC. The molecular pathology of breast cancer progression. J Pathol. 2011; 223: 308-318. [CrossRef]
  29. Zhong X, Heinicke F, Rayner S. miRBaseMiner, a tool for investigating miRBase content. RNA Biol. 2019; 16: 1534-1546. [CrossRef]
  30. Deng L, Guo P, Han D, Tan W. Sensing miRNAs for disease diagnostics. Anal Sens. 2023; 3: e202200083. [CrossRef]
  31. Zheng X, Xu S, Zhang Y, Huang X. Nucleotide-level convolutional neural networks for pre-miRNA classification. Sci Rep. 2019; 9: 628. [CrossRef]
  32. Sohail AM, Khawar MB, Afzal A, Hassan A, Shahzaman S, Ali A. Multifaceted roles of extracellular RNAs in different diseases. Mil Med Res. 2022; 9: 43. [CrossRef]
  33. Kosaka N, Iguchi H, Yoshioka Y, Takeshita F, Matsuki Y, Ochiya T. Secretory mechanisms and intercellular transfer of microRNAs in living cells. J Biol Chem. 2010; 285: 17442-17452. [CrossRef]
  34. Geekiyanage H, Rayatpisheh S, Wohlschlegel JA, Brown Jr R, Ambros V. Extracellular microRNAs in human circulation are associated with miRISC complexes that are accessible to anti-AGO2 antibody and can bind target mimic oligonucleotides. Proc Natl Acad Sci. 2020; 117: 24213-24223. [CrossRef]
  35. Arroyo JD, Chevillet JR, Kroh EM, Ruf IK, Pritchard CC, Gibson DF, et al. Argonaute2 complexes carry a population of circulating microRNAs independent of vesicles in human plasma. Proc Natl Acad Sci. 2011; 108: 5003-5008. [CrossRef]
  36. Schröder R, Illert AL, Erbes T, Flotho C, Lübbert M, Duque-Afonso J. The epigenetics of breast cancer-opportunities for diagnostics, risk stratification and therapy. Epigenetics. 2022; 17: 612-624. [CrossRef]
  37. Zou R, Loke SY, Tang YC, Too HP, Zhou L, Lee AS, et al. Development and validation of a circulating microRNA panel for the early detection of breast cancer. Br J Cancer. 2022; 126: 472-481. [CrossRef]
  38. Erturk E, Onur OE, Akgun O, Tuna G, Yildiz Y, Ari F. Mitochondrial miRNAs (MitomiRs): Their potential roles in breast and other cancers. Mitochondrion. 2022; 66: 74-81. [CrossRef]
  39. Cosentino G, Plantamura I, Iorio MV. Pathophysiology rolesr and translational opportunities of miRNAs in breast cancer. In: MicroRNA in human malignancies. Cambridge, MA: Academic Press; 2022. pp. 195-201. [CrossRef]
  40. Shaban NZ, Ibrahim NK, Saada HN, El-Rashidy FH, Shaaban HM, Farrag MA, et al. miR-34a and miR-21 as biomarkers in evaluating the response of chemo-radiotherapy in Egyptian breast cancer patients. J Radiat Res Appl Sci. 2022; 15: 285-292. [CrossRef]
  41. Weng S, Lin D, Lai S, Tao H, Chen T, Peng M, et al. Highly sensitive and reliable detection of microRNA for clinically disease surveillance using SERS biosensor integrated with catalytic hairpin assembly amplification technology. Biosens Bioelectron. 2022; 208: 114236. [CrossRef]
  42. Tripathi SK, Mathaiyan J, Kayal S, Ganesh RN. Identification of differentially expressed Mirna by next generation sequencing in locally advanced breast cancer patients of south Indian origin. Asian Pac J Cancer Prev. 2022; 23: 2255-2261. [CrossRef]
  43. Del’haye GG, Nulmans I, Bouteille SP, Sermon K, Wellekens B, Rombaut M, et al. Development of an adverse outcome pathway network for breast cancer: A comprehensive representation of the pathogenesis, complexity and diversity of the disease. Arch Toxikol. 2022; 96: 2881-2897. [CrossRef]
  44. Wei J, Lu Y, Wang R, Xu X, Liu Q, He S, et al. MicroRNA-375: Potential cancer suppressor and therapeutic drug. Biosci Rep. 2021; 41: BSR20211494. [CrossRef]
  45. Maciak K, Dziedzic A, Miller E, Saluk-Bijak J. miR-155 as an important regulator of multiple sclerosis pathogenesis. A review. Int J Mol Sci. 2021; 22: 4332. [CrossRef]
  46. Seeliger C, Krauss T, Honecker J, Mengel LA, Buekens L, Mesas-Fernández A, et al. miR-375 is cold exposure sensitive and drives thermogenesis in visceral adipose tissue derived stem cells. Sci Rep. 2022; 12: 9557. [CrossRef]
  47. Wu Y, Hong Q, Lu F, Zhang Z, Li J, Nie Z, et al. The diagnostic and prognostic value of miR-155 in cancers: An updated meta-analysis. Mol Diagn Ther. 2023; 27: 283-301. [CrossRef]
  48. Faraoni I, Antonetti FR, Cardone J, Bonmassar E. miR-155 gene: A typical multifunctional microRNA. Biochim Biophys Acta Mol Basis Dis. 2009; 1792: 497-505. [CrossRef]
  49. Li B, Liu S, Yang Q, Li Z, Li J, Wu J, et al. Macrophages in tumor-associated adipose microenvironment accelerate tumor progression. Adv Biol. 2023; 7: 2200161. [CrossRef]
  50. Chen H, Xie G, Luo Q, Yang Y, Hu S. Regulatory miRNAs, circRNAs and lncRNAs in cell cycle progression of breast cancer. Funct Integr Genomics. 2023; 23: 233. [CrossRef]
  51. Motlagh FM, Kadkhoda S, Motamedrad M, Javidzade P, Khalilian S, Modarressi MH, et al. Roles of non-coding RNAs in cell death pathways involved in the treatment of resistance and recurrence of cancer. Pathol Res Pract. 2023; 247: 154542. [CrossRef]
  52. Hussen BM, Abdullah KH, Abdullah SR, Majeed NM, Mohamadtahr S, Rasul MF, et al. New insights of miRNA molecular mechanisms in breast cancer brain metastasis and therapeutic targets. Non-coding RNA Res. 2023; 8: 645-660. [CrossRef]
  53. Chen HH, Hao PH, Zhang FY, Zhang TN. Non-coding RNAs in metabolic reprogramming of bone and soft tissue sarcoma: Fundamental mechanism and clinical implication. Biomed Pharmacother. 2023; 160: 114346. [CrossRef]
  54. Chengizkhan G, Thangavelu SK, Muthusami S, Banerjee A, Pathak S, Natarajan G, et al. Regulation of cancer stemness, cell signaling, reactive oxygen species, and microRNAs in cancer stem cells. In: Cancer stem cells and signaling pathways. Cambridge, MA: Academic Press; 2024. pp. 243-263. [CrossRef]
  55. Biswal P, Lalruatfela A, Behera SK, Biswal S, Mallick B. miR-203a-A multifaceted regulator modulating cancer hallmarks and therapy response. IUBMB Life. 2023. doi: 10.1002/iub.2786. [CrossRef]
  56. Hu Q, Zhang X, Sun M, Zhang Z, Sun D. Potential epigenetic molecular regulatory networks in ocular neovascularization. Front Genet. 2022; 13: 970224. [CrossRef]
  57. Carlsen L, Zhang S, Tian X, De La Cruz A, George A, Arnoff TE, et al. The role of p53 in anti-tumor immunity and response to immunotherapy. Front Mol Biosci. 2023; 10: 1148389. [CrossRef]
  58. Frisbie L, Buckanovich RJ, Coffman L. Carcinoma-associated mesenchymal stem/stromal cells: Architects of the pro-tumorigenic tumor microenvironment. Stem Cells. 2022; 40: 705-715. [CrossRef]
  59. Mansoori B, Kiani S, Mezajin AA, Zandi P, Banaie H, Rostamzadeh D, et al. MicroRNA-143-5p suppresses ER-positive breast cancer development by targeting oncogenic HMGA2. Clin Breast Cancer. 2023; 23: e480-e490.e3. [CrossRef]
  60. Ismail A, El-Mahdy HA, Abulsoud AI, Sallam AA, Eldeib MG, Elsakka EG, et al. Beneficial and detrimental aspects of miRNAs as chief players in breast cancer: A comprehensive review. Int J Biol Macromol. 2023; 224: 1541-1565. [CrossRef]
  61. Anilkumar KV, Rema LP, John MC, Vanesa John T, George A. miRNAs in the prognosis of triple-negative breast cancer: A review. Life Sci. 2023; 333: 122183. [CrossRef]
  62. De Summa S, Traversa D, Daniele A, Palumbo O, Carella M, Stallone R, et al. miRNA deregulation and relationship with metabolic parameters after mediterranean dietary intervention in BRCA-mutated women. Front Oncol. 2023; 13: 1147190. [CrossRef]
  63. Chhichholiya Y, Singh HV, Singh S, Munshi A. Genetic variations in tumor-suppressor miRNA-encoding genes and their target genes: Focus on breast cancer development and possible therapeutic strategies. Clin Transl Oncol. 2023; 26: 24. [CrossRef]
  64. Nemeth K, Bayraktar R, Ferracin M, Calin GA. Non-coding RNAs in disease: From mechanisms to therapeutics. Nat Rev Genet. 2023. doi: 10.1038/s41576-023-00662-1. [CrossRef]
  65. Tluli O, Al-Maadhadi M, Al-Khulaifi AA, Akomolafe AF, Al-Kuwari SY, Al-Khayarin R, et al. Exploring the role of microRNAs in glioma progression, prognosis, and therapeutic strategies. Cancers. 2023; 15: 4213. [CrossRef]
  66. Heneghan HM, Miller N, Lowery AJ, Sweeney KJ, Newell J, Kerin MJ. Circulating microRNAs as novel minimally invasive biomarkers for breast cancer. Ann Surg. 2010; 251: 499-505. [CrossRef]
  67. Roth C, Rack B, Müller V, Janni W, Pantel K, Schwarzenbach H. Circulating microRNAs as blood-based markers for patients with primary and metastatic breast cancer. Breast Cancer Res. 2010; 12: R90. [CrossRef]
  68. Shi L, Li J, Xiang Q, Tan Y, Zhang H, Liu S, et al. A dual-ratio fluorescent probe with a single excitation triple-signal to synchronously detect PTK7 and miRNA-21 for breast cancer early diagnosis. Biosens Bioelectron. 2023; 237: 115529. [CrossRef]
  69. Zhou X, Zhang J, Jia Q, Ren Y, Wang Y, Shi L, et al. Reduction of miR-21 induces glioma cell apoptosis via activating caspase 9 and 3. Oncol Rep. 2010; 24: 195-201. [CrossRef]
  70. Cao G, Long K, Qiu Y, Peng L, Han H, Wang Y, et al. A light-up fluorescence platform based DNA: RNA hybrid G-quadruplet for detecting single nucleotide variant of ctDNA and miRNA-21. Talanta. 2023; 257: 124373. [CrossRef]
  71. Liu R, Liu C, He X, Sun P, Zhang B, Yang H, et al. MicroRNA-21 promotes pancreatic β cell function through modulating glucose uptake. Nat Commun. 2022; 13: 3545. [CrossRef]
  72. Li N, Wang X, Sun J, Liu Y, Han A, Lin Z, et al. miR-21-5p/Tiam1-mediated glycolysis reprogramming drives breast cancer progression via enhancing PFKL stabilization. Carcinogenesis. 2022; 43: 705-715. [CrossRef]
  73. Wang J, Wang Q, Guan Y, Sun Y, Wang X, Lively K, et al. Breast cancer cell-derived microRNA-155 suppresses tumor progression via enhancing immune cell recruitment and antitumor function. J Clin Invest. 2022; 132: e157248. [CrossRef]
  74. Kai QI, Fei YE, Guiyuan GU, Teng BE, Songhua LU. Correlation of DCE-MRI parameters and expression of miR-27 and miR-155 with breast cancer. Imaging Sci Photochem. 2022; 40. doi: 10.7517/issn.1674-0475.210917.
  75. Xu Q, Xu JL, Chen WQ, Xu WX, Song YX, Tang WJ, et al. Roles and mechanisms of miR-195-5p in human solid cancers. Biomed Pharmacother. 2022; 150: 112885. [CrossRef]
  76. Yang R, Xing L, Zheng X, Sun Y, Wang X, Chen J. Retraction note to: The circRNA circAGFG1 acts as a sponge of miR-195-5p to promote triple-negative breast cancer progression through regulating CCNE1 expression. Mol Cancer. 2019; 18: 4. [CrossRef]
  77. Patel N, Garikapati KR, Makani VK, Pal S, Vangara N, Bhadra MP. miRNA let-7a inhibits invasion, migration, anchorage-independent growth by suppressing EZH2 and promotes mesenchymal to epithelial transition in MDAMB-231. Gene Rep. 2023; 31: 101752. [CrossRef]
  78. Selem NA, Nafae H, Manie T, Youness RA, Gad MZ. Let-7a/cMyc/CCAT1/miR-17-5p circuit re-sensitizes atezolizumab resistance in triple negative breast cancer through modulating PD-L1. Pathol Res Pract. 2023; 248: 154579. [CrossRef]
  79. Zhang Y, Li S, Peng C, Shi Z, Miao X. Dumbbell hybridization chain reaction coupled with positively charged Au@ luminol nanoparticles for enhanced electrochemiluminescent sensing of exosomal miRNA-21. Bioelectrochemistry. 2023; 155: 108556. [CrossRef]
  80. Guo F, Zhu X, Zhao Q, Huang Q. miR-589-3p sponged by the lncRNA TINCR inhibits the proliferation, migration and invasion and promotes the apoptosis of breast cancer cells by suppressing the Akt pathway via IGF1R. Int J Mol Med. 2020; 46: 989-1002. [CrossRef]
  81. Sameti P, Amini M, Oroojalian F, Baghay Esfandyari Y, Tohidast M, Rahmani SA, et al. MicroRNA-425: A pivotal regulator participating in tumorigenesis of human cancers. Mol Biotechnol. 2023. doi: 10.1007/s12033-023-00756-5. [CrossRef]
  82. Imani S, Wu RC, Fu J. MicroRNA-34 family in breast cancer: From research to therapeutic potential. J Cancer. 2018; 9: 3765-3775. [CrossRef]
  83. Li M, Zhou Y, Xia T, Zhou X, Huang Z, Zhang H, et al. Circulating microRNAs from the miR-106a-363 cluster on chromosome X as novel diagnostic biomarkers for breast cancer. Breast Cancer Res Treat. 2018; 170: 257-270. [CrossRef]
  84. Alhasan L. MiR-126 modulates angiogenesis in breast cancer by targeting VEGF-A-mRNA. Asian Pac J Cancer Prev. 2019; 20: 193-197. [CrossRef]
  85. Wang Q, Ye B, Wang P, Yao F, Zhang C, Yu G. Overview of microRNA-199a regulation in cancer. Cancer Manag Res. 2019; 11: 10327-10335. [CrossRef]
  86. Ye L, Wang F, Wu H, Yang H, Yang Y, Ma Y, et al. Functions and targets of miR-335 in cancer. Onco Targets Ther. 2021; 14: 3335-3349. [CrossRef]
  87. Kim J, Park S, Hwang D, Kim SI, Lee H. Diagnostic value of circulating miR-202 in early-stage breast cancer in South Korea. Medicina. 2020; 56: 340. [CrossRef]
  88. Dai W, He J, Zheng L, Bi M, Hu F, Chen M, et al. miR-148b-3p, miR-190b, and miR-429 regulate cell progression and act as potential biomarkers for breast cancer. J Breast Cancer. 2019; 22: 219-236. [CrossRef]
  89. Ahmed R, Samanta S, Banerjee J, Kar SS, Dash SK. Modulatory role of miRNAs in thyroid and breast cancer progression and insights into their therapeutic manipulation. Curr Res Pharmacol Drug Discov. 2022; 3: 100131. [CrossRef]
  90. Selcuklu SD, Donoghue MT, Rehmet K, de Souza Gomes M, Fort A, Kovvuru P, et al. MicroRNA-9 inhibition of cell proliferation and identification of novel miR-9 targets by transcriptome profiling in breast cancer cells. J Biol Chem. 2012; 287: 29516-29528. [CrossRef]
  91. Tang W, Li GS, Li JD, Pan WY, Shi Q, Xiong DD, et al. The role of upregulated miR-375 expression in breast cancer: An in vitro and in silico study. Pathol Res Pract. 2020; 216: 152754. [CrossRef]
  92. Wang Z, Hu S, Li X, Liu Z, Han D, Wang Y, et al. MiR-16-5p suppresses breast cancer proliferation by targeting ANLN. BMC Cancer. 2021; 21: 1188. [CrossRef]
  93. Amini S, Abak A, Estiar MA, Montazeri V, Abhari A, Sakhinia E. Expression analysis of MicroRNA-222 in breast cancer. Clin Lab. 2018; 64: 491-496. [CrossRef]
  94. Chirshev E, Oberg KC, Ioffe YJ, Unternaehrer JJ. Let-7 as biomarker, prognostic indicator, and therapy for precision medicine in cancer. Clin Transl Med. 2019; 8: 24. [CrossRef]
  95. Luengo-Gil G, Gonzalez-Billalabeitia E, Perez-Henarejos SA, Navarro Manzano E, Chaves-Benito A, Garcia-Martinez E, et al. Angiogenic role of miR-20a in breast cancer. PLoS One. 2018; 13: e0194638. [CrossRef]
  96. Wang Y, Zeng G, Jiang Y. The emerging roles of miR-125b in cancers. Cancer Manag Res. 2020; 12: 1079-1088. [CrossRef]
  97. Zheng J, Xu T, Chen F, Zhang Y. MiRNA-195-5p functions as a tumor suppressor and a predictive of poor prognosis in non-small cell lung cancer by directly targeting CIAPIN1. Pathol Oncol Res. 2019; 25: 1181-1190. [CrossRef]
  98. Wang T, Zhang H, Wang H, Chang C, Huang F, Zhang L. MiR-505-5p inhibits proliferation and promotes apoptosis of osteosarcoma cells via regulating RASSF8 expression. J BUON. 2021; 26: 599-605.
  99. Matamala N, Vargas MT, Gonzalez-Campora R, Minambres R, Arias JI, Menendez P, et al. Tumor microRNA expression profiling identifies circulating microRNAs for early breast cancer detection. Clin Chem. 2015; 61: 1098-1106. [CrossRef]
  100. Asadirad A, Khodadadi A, Talaiezadeh A, Shohan M, Rashno M, Joudaki N. Evaluation of miRNA-21-5p and miRNA-10b-5p levels in serum-derived exosomes of breast cancer patients in different grades. Mol Cell Probes. 2022; 64: 101831. [CrossRef]
  101. Ljepoja B, García-Roman J, Sommer AK, Wagner E, Roidl A. MiRNA-27a sensitizes breast cancer cells to treatment with selective estrogen receptor modulators. Breast. 2019; 43: 31-38. [CrossRef]
  102. Moghbeli M, Zangouei AS, Nasrpour Navaii Z, Taghehchian N. Molecular mechanisms of the microRNA-132 during tumor progressions. Cancer Cell Int. 2021; 21: 439. [CrossRef]
  103. Wei XC, Lv ZH. MicroRNA-132 inhibits migration, invasion and epithelial-mesenchymal transition via TGFβ1/Smad2 signaling pathway in human bladder cancer. OncoTargets Ther. 2019; 12: 5937-5945. [CrossRef]
  104. Yang C, Dou R, Yin T, Ding J. MiRNA-106b-5p in human cancers: Diverse functions and promising biomarker. Biomed Pharmacother. 2020; 127: 110211. [CrossRef]
  105. Cao X, Zhang J, Apaer S, Yao G, Li T. microRNA-19a-3p and microRNA-376c-3p promote hepatocellular carcinoma progression through SOX6-mediated Wnt/β-catenin signaling pathway. Int J Gen Med. 2021; 14: 89-102. [CrossRef]
  106. Cardinali B, Tasso R, Piccioli P, Ciferri MC, Quarto R, Del Mastro L. Circulating miRNAs in breast cancer diagnosis and prognosis. Cancers. 2022; 14: 2317. [CrossRef]
  107. Alkhathami AG, Verma AK, Alfaifi M, Kumar L, Alshahrani MY, Hakami AR, et al. Role of miRNA-495 and NRXN-1 and CNTN-1 mRNA expression and its prognostic importance in breast cancer patients. J Oncol. 2021; 2021: 9657071. [CrossRef]
  108. Zhang J, Cao Z, Yang G, You L, Zhang T, Zhao Y. MicroRNA-27a (miR-27a) in solid tumors: A review based on mechanisms and clinical observations. Front Oncol. 2019; 9: 893. [CrossRef]
  109. Seddik MI, Osama O, Jabir MA, Abdelrahman EM, Nigm DA. Diagnostic values of microRNA 27a in breast cancer patients. Egypt J Immunol. 2021; 28: 127-137. [CrossRef]
  110. Garrido-Cano I, Pattanayak B, Adam-Artigues A, Lameirinhas A, Torres-Ruiz S, Tormo E, et al. MicroRNAs as a clue to overcome breast cancer treatment resistance. Cancer Metastasis Rev. 2022; 41: 77-105. [CrossRef]
  111. Rahimi M, Sharifi-Zarchi A, Zarghami N, Geranpayeh L, Ebrahimi M, Alizadeh E. Down-regulation of miR-200c and up-regulation of miR-30c target both stemness and metastasis genes in breast cancer. Cell J. 2020; 21: 467-478.
  112. Gong J, Jaiswal R, Mathys JM, Combes V, Grau GE, Bebawy M. Microparticles and their emerging role in cancer multidrug resistance. Cancer Treat Rev. 2012; 38: 226-234. [CrossRef]
  113. Li H, Yang BB. Friend or foe: The role of microRNA in chemotherapy resistance. Acta Pharmacol Sin. 2013; 34: 870-879. [CrossRef]
  114. Dentelli P, Traversa M, Rosso A, Togliatto G, Olgasi C, Marchiò C, et al. miR-221/222 control luminal breast cancer tumor progression by regulating different targets. Cell Cycle. 2014; 13: 1811-1826. [CrossRef]
  115. Faldoni FL, Rainho CA, Rogatto SR. Epigenetics in inflammatory breast cancer: Biological features and therapeutic perspectives. Cells. 2020; 9: 1164. [CrossRef]
  116. Ozyurt R, Ozpolat B. Molecular mechanisms of anti-estrogen therapy resistance and novel targeted therapies. Cancers. 2022; 14: 5206. [CrossRef]
  117. Di Leva G, Cheung DG, Croce CM. miRNA clusters as therapeutic targets for hormone-resistant breast cancer. Expert Rev Endocrinol Metab. 2015; 10: 607-617. [CrossRef]
  118. García-Becerra R, Santos N, Díaz L, Camacho J. Mechanisms of resistance to endocrine therapy in breast cancer: Focus on signaling pathways, miRNAs and genetically based resistance. Int J Mol Sci. 2012; 14: 108-145. [CrossRef]
  119. Budi HS, Younus LA, Lafta MH, Parveen S, Mohammad HJ, Al-Qaim ZH, et al. The role of miR-128 in cancer development, prevention, drug resistance, and immunotherapy. Front Oncol. 2023; 12: 1067974. [CrossRef]
  120. Giovannetti E, Erozenci A, Smit J, Danesi R, Peters GJ. Molecular mechanisms underlying the role of microRNAs (miRNAs) in anticancer drug resistance and implications for clinical practice. Crit Rev Oncol Hematol. 2012; 81: 103-122. [CrossRef]
  121. Tamang S, Acharya V, Roy D, Sharma R, Aryaa A, Sharma U, et al. SNHG12: An LncRNA as a potential therapeutic target and biomarker for human cancer. Front Oncol. 2019; 9: 901. [CrossRef]
  122. Ren Y, Zhou X, Mei M, Yuan XB, Han L, Wang GX, et al. MicroRNA-21 inhibitor sensitizes human glioblastoma cells U251 (PTEN-mutant) and LN229 (PTEN-wild type) to taxol. BMC Cancer. 2010; 10: 27. [CrossRef]
  123. Kaboli PJ, Rahmat A, Ismail P, Ling KH. MicroRNA-based therapy and breast cancer: A comprehensive review of novel therapeutic strategies from diagnosis to treatment. Pharmacol Res. 2015; 97: 104-121. [CrossRef]
  124. Tormo E, Pineda B, Serna E, Guijarro A, Ribas G, Fores J, et al. MicroRNA profile in response to doxorubicin treatment in breast cancer. J Cell Biochem. 2015; 116: 2061-2073. [CrossRef]
  125. Usmani A, Shoro AA, Shirazi B, Memon Z. Investigative and extrapolative role of microRNAs’ genetic expression in breast carcinoma. Pak J Med Sci. 2016; 32: 766-772. [CrossRef]
  126. Alzhrani R, Alsaab HO, Petrovici A, Bhise K, Vanamala K, Sau S, et al. Improving the therapeutic efficiency of noncoding RNAs in cancers using targeted drug delivery systems. Drug Discov Today. 2020; 25: 718-730. [CrossRef]
  127. Ali Syeda Z, Langden SS, Munkhzul C, Lee M, Song SJ. Regulatory mechanism of microRNA expression in cancer. Int J Mol Sci. 2020; 21: 1723. [CrossRef]
  128. Anwar M, Muhammad F, Akhtar B. Biodegradable nanoparticles as drug delivery devices. J Drug Deliv Sci Technol. 2021; 64: 102638. [CrossRef]
  129. Bravo-Vázquez LA, Méndez-García A, Rodríguez AL, Sahare P, Pathak S, Banerjee A, et al. Applications of nanotechnologies for miRNA-based cancer therapeutics: Current advances and future perspectives. Front Bioeng Biotechnol. 2023; 11: 1208547. [CrossRef]
  130. Amaldoss MJ, Yang JL, Koshy P, Unnikrishnan A, Sorrell CC. Inorganic nanoparticle-based advanced cancer therapies: Promising combination strategies. Drug Discov Today. 2022; 27: 103386. [CrossRef]
  131. Akinc A, Maier MA, Manoharan M, Fitzgerald K, Jayaraman M, Barros S, et al. The Onpattro story and the clinical translation of nanomedicines containing nucleic acid-based drugs. Nat Nanotechnol. 2019; 14: 1084-1087. [CrossRef]
  132. Bader AG, Brown D, Stoudemire J, Lammers P. Developing therapeutic microRNAs for cancer. Gene Ther. 2011; 18: 1121-1126. [CrossRef]
  133. Grimaldi AM, Salvatore M, Incoronato M. miRNA-based therapeutics in breast cancer: A systematic review. Front Oncol. 2021; 11: 668464. [CrossRef]
  134. Wang J, Xu F, Zhu X, Li X, Li Y, Li J. Targeting microRNAs to regulate the integrity of the blood-brain barrier. Front Bioeng Biotechnol. 2021; 9: 673415. [CrossRef]
  135. Fu Z, Wang L, Li S, Chen F, Au-Yeung KK, Shi C. MicroRNA as an important target for anticancer drug development. Front Pharmacol. 2021; 12: 736323. [CrossRef]
  136. Radwan AF, Shaker OG, El-Boghdady NA, Senousy MA. Association of MALAT1 and PVT1 variants, expression profiles and target miRNA-101 and miRNA-186 with colorectal cancer: Correlation with epithelial-mesenchymal transition. Int J Mol Sci. 2021; 22: 6147. [CrossRef]
  137. Fakhry MM, Abdel-Hamed AR, Abo-elmatty DM, Mesbah NM, Al-Sawaf A, Ezzat O, et al. A possible novel co-relation of locus 7q11 rs1761667 polymorphism with the severity of preeclampsia in Egyptian pregnant women. Meta Gene. 2020; 24: 100650. [CrossRef]
Download PDF Download Citation
0 0