The disorder known as breast cancer is complex and is marked by a variety of genetic changes. With the exception of skin cancers, breast cancer is the most common cancer among women, accounting for about one in three cancer diagnoses among US women, according to the American Cancer Society. The previous ten years have seen major technological developments that have aided in the researchers’ deeper understanding of this complicated illness. There are six main subtypes of breast cancer, based on the phenotypic and gene expression profile. Luminal A, B, tumor improved with human epidermal growth factor receptor 2 (Her2), basal-like, normal-like, and claudin-low subtypes are the six main subtypes. The most predominant subtype among them is luminal A, which is notable by the expression of the progesterone receptor (PR), estrogen receptor (ER), Bcl-2, and lack of Her2. It makes up between 50 and 60 percent of all cases of breast cancer (Singh & Mo, 2013). The lack of Her2 and the existence of PR and ER describe the luminal B subtype. Their increased proliferation rate, indicated by strong Ki67 staining, allows them to be distinguished from the luminal A subtype (Cheang et al., 2009). One family of endogenous small RNAs known as microRNAs (miRNAs) has exposed a new degree of gene control in cells. They are also widely distributed in the genomes of high eukaryotic cells and help as essential parts of the central dogma machinery. It is estimated that miRNA genes account for 1% to 2% of all eukaryotic genes (Chalfie et al., 1981) It has been confirmed that they regulator important gene activation and suppression mechanisms, numerous pathways including the control of several genes can be coordinated by a single miRNA. Equally, a single miRNA target can be under the mutual control of multiple distinct miRNAs. This varied function facilitates the intricate network of eukaryotic cell activity by paying to the intricacy of gene regulation(Kim & Nam, 2006). Including the development of organs, apoptosis, cell division, and hematopoietic cell differentiation (Bartel, 2004).
Several studies have been carried out to determine the miRNAs that display differential expression and govern the beginning and progression of breast cancer across various subtypes of the disease. 29 miRNAs with knowingly dysregulated expression were found through miRNA study of 76 breast cancer and 10 normal breast samples. The most pointedly dysregulated miRNAs were miR-125b, miR-145, miR-21, and miR-155, and 15 of them were able to exactly predict whether the sample under analysis was a tumor or normal breast tissue (Iorio et al., 2005). miRNAs such as let-7, miR-17/20, miR-22, miR-31, miR-126, miR-145, miR-146, miR-206, miR-335, and miR-448 role as metastasis suppressors in breast cancer. To highlight the role of these genes in metastasis, we have chosen a few miRNA targets (Cheang et al., 2009). The ability of miR-7 to aim the epidermal growth factor receptor (EGFR), which controls acute cellular processes including proliferation and differentiation and is frequently overexpressed in various malignancies, including breast cancer, has been linked to its potential to limit metastasis (Webster et al., 2009). Additionally, miR-7 has the ability to suppress the expression of p21-activated kinase 1, a signaling kinase associated in a number of malignancies. The highly aggressive and oncogenic breast cancer cell line MDA-MB-231 displays decreased invasion capacity, motility, anchorage independence, and carcinogenesis as a result of overexpressing miR-7 (Reddy et al., 2008). Different forms of cancer may use miR-17 as an oncogenic miRNA, miR-17/20 has been exposed to target cyclin D1, a cell cycle controlling subunit that permits the G1-S phase transition. It has been observed that ~50% of human breast tumors had increased cyclin D1 expression, which is contrariwise correlated with miR-17/20. In breast cancer cell lines, overexpression of miR-17/20 inhibits cell growth and stops the cell cycle at the G1 phase (Singh & Mo, 2013). Furthermore, vital expression of miR-30 targets ITGB3 expression to cause cell death and inhibits the capacity of BT-ICs to self-renew through Ubc9. BT-IC xenograft overexpressing miR-30, in certain, can decrease lung metastasis and tumorigenesis in a model of non-obese diabetic/severe mutual immunodeficient (NOD/SCID) mice (Yu et al., 2010). Tumor suppressor miRNAs like miR-145 are well-known and have the capability to target numerous genes, including IRS-1, mucin-1, c-myc, JAM-A, and fascin. Directing multiple significant suppressors of carcinogenesis and metastasis is within the boundaries of miR-146. MiR-146, when naturally expressed in the metastatic breast cancer cell line MDA-MB-231, inhibits NFκB by downregulating TNF related factor 6 and interleukin receptor associated kinase (Singh & Mo, 2013).
The proportion of cells that can initiate a new tumor and are frequently resistant to mutual chemotherapeutic treatments is one of the main blocks to treating breast cancer (Smalley et al., 2013). These are breast cancer stem cells and they are regularly identified by their capacity to twitch tumors in immunocompromised or syngeneic mice, their capacity to self-renew as directed by the development of tumors in secondary mice, and their ability to differentiate into the non-self-renewing cells that make up the bulk of the tumor (McDermott & Wicha, 2010). It has been proposed that miRNAs sustain the protection of stem cell or tumor-initiating characteristics, and that a particular miRNA expression pattern can expect the different aspects of breast cancer, including metastasis(Wang et al., 2012).
