A new strategy for gene regulator was created over two decades ago with the finding of microRNAs, or miRNAs. These small non-coding RNAs have been associated to almost all known physiological and pathological processes, including cancer, over the past ten years. MiRNAs can be dysregulated in cancer, much like several important protein-coding genes. In this case, they can act as a group to indicate segregating states or as individual oncogenes or tumour suppressors. Importantly, miRNA biology can be used therapeutically as a drug target or as the medicine itself, or it can be exploited experimentally to study cancer characteristics (Lujambio & Lowe, 2012). MicroRNAs, or small non-coding RNAs with an evolutionary conserved length of 18–25 nucleotides, play a vital role in the regulation of gene expression in the cells. The ribonucleases Drosha and Dicer1 chronologically digest a longer primary miRNA (pri-miRNA) transcript to produce mature miRNA products. In 1993, miRNAs were initially identified as developmental time regulators in Caenorhabditis elegans (Lee et al., 1993). Nearly all cancer cells use miRNAs to control the expression of certain genes. These cells display altered miRNA expression profiles, and new research suggests that these designs may help better categorize malignancies and estimate their behavior. Additionally, it has now been verified that miRNAs function as cancer “drivers” in a way alike to that of protein-coding genes, whose changes importantly and actively stimulus the development of cancer and its malignant conversion. Subsequently miRNAs can alter hundreds of target genes, they are attractive more significant players in the directive of the “hallmarks” of cancer (Hanahan & Weinberg, 2011). miRNA cluster was frequently removed or knockdown in chronic lymphocytic leukemia, as initially shown by Croce and colleagues in 2002. This study opened the access for a more thorough analysis of miRNA loss or amplification in tumors and proposed that non-coding genes may play a role in the onset of cancer. It was later confirmed that miRNAs were expressed differently in cancer cells, resulting in the formation of typical and individual miRNA expression patterns(Lu et al., 2005) The extensive downregulation of miRNAs in cancer cells has been credited to two primary processes. One is the practice of oncogenic transcription factors to inhibit transcription. For example, it is currently unclear how much the MYC oncoprotein, which is overexpressed in many malignancies, transcriptionally represses specific miRNAs to cause cancer or to replicate a secondary consequence (Chang et al., 2008). The other theory is based on the reflection that mechanisms in the miRNA biogenesis pathway are regularly absent or exhibit changed activity in cancer cells, and it entails modifications to miRNA production(Thomson et al., 2006). TP53 tumour suppressor is debatably the most significant and extensively researched cancer gene, it is not unforeseen that a number of studies have indicated that miRNA biology may be involved in the regulation and activity of this gene. As a sequence-specific DNA-binding protein, the p53 protein has the capability to both stimulate and repress transcription. p53 can transactivate many miRNAs in addition to its ability to influence canonical protein-coding targets like CDKN1A and PUMA, which certainly accounts for the majority of its actions. The miR-34 family, which overcomes genes that may stimulate cell death and cell proliferation, is one of the best-studied classes. These genes are probable targets in a p53-mediated tumor-suppressor response (He et al., 2007). miRNAs have the capability to influence mechanisms that aid in the spread of cancer, such as metastasis, in addition to reassuring the start of the disease. Modifications to the RNA interference (RNAi) gear on a global scale or impacts on the transcription of miRNAs can change their levels, and both processes appear to be crucial for this process. For example, miR-10b and miR-9 have the capability to cause metastasis in breast cancer, while miR-126, miR-335, and miR-31 function as suppressors. The epithelial-to-mesenchymal transition is repressed by the miR-200 family, which affects one part of the metastatic process. However, miR-200 may additionally enable the colonization of metastatic cells in breast cancer, thereby offering an additional illustration of the antagonistic actions of certain miRNAs. On the other hand, in experimental models of head and neck squamous-cell carcinomas, lung adenocarcinomas, and breast malignancies, lower levels of certain miRNAs subsequent from Dicer1 downregulation also facilitate cell motility and are linked to increased metastasis (Lujambio & Lowe, 2012).
