Abstract
MicroRNAs (miRNAs) are endogenous non-coding small RNAs that downregulate target gene expression by imperfect base-pairing with the 3′ untranslated regions (3′UTRs) of target gene mRNAs. MiRNAs play important roles in regulating cancer cell proliferation, stemness maintenance, tumorigenesis, cancer metastasis, and cancer therapeutic resistance. While studies have shown that dysregulation of miRNA-205-5p (miR-205) expression is controversial in different types of human cancers, it is generally observed that miR-205-5p expression level is downregulated in breast cancer and that miR-205-5p exhibits a tumor suppressive function in breast cancer. This review focuses on the role of miR-205-5p dysregulation in different subtypes of breast cancer, with discussions on the effects of miR-205-5p on breast cancer cell proliferation, epithelial–mesenchymal transition (EMT), metastasis, stemness and therapy-resistance, as well as genetic and epigenetic mechanisms that regulate miR-205-5p expression in breast cancer. In addition, the potential diagnostic and therapeutic value of miR-205-5p in breast cancer is also discussed. A comprehensive list of validated miR-205-5p direct targets is presented. It is concluded that miR-205-5p is an important tumor suppressive miRNA capable of inhibiting the growth and metastasis of human breast cancer, especially triple negative breast cancer. MiR-205-5p might be both a potential diagnostic biomarker and a therapeutic target for metastatic breast cancer.
Highlights
Breast cancer is posing a tremendous threat to women’s health globally, and is the most prevalent female malignancy in the world [1]
Advancements in technology has allowed breast cancer to be further classified into different subtypes based upon molecular markers defined by immunohistochemistry (IHC): Estrogen (ER)/progesterone (PR), human epidermal growth factor receptor 2 (HER2), or triple negative breast cancer [2]
This is especially true for triple negative breast cancer (TNBC), which is defined as estrogen receptor (ER), progesterone receptor (PR), and HER2 negative
Summary
Breast cancer is posing a tremendous threat to women’s health globally, and is the most prevalent female malignancy in the world [1]. It has been reported that miRNAs participate in cancer initiation, tumorigenesis, proliferation, metastasis, epithelial mesenchymal transition (EMT), stemness maintenance, and therapeutic resistance by downregulating target oncogenes or tumor suppressive genes. As a first-line endocrine therapy for ER/PR+ breast cancers, binds to the estrogen receptor to competitively block estrogen-induced target gene expression, which leads to suppression of cancer cell proliferation [50]. Studies have shown that AMOT activates the ERK1/2 pathway to drive cell proliferation in ER+ breast cancer [54], and that miR-205-5p inhibits cell growth by direct targeting of AMOT in MCF-7 breast cancer cells [55]. Recent studies have shown that miR-205-5p directly targets HER3 This results in the inhibition of proliferation in SKBr3, MCF7, and MDA-MB-231 breast cancer cell lines [40,42]. This group determined that p63 is a direct target of miR-205-5p, and there is a feedback loop between p63 and miR-205-5p, which determines some of the features of BCSCs [69]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
