• The miRNA molecules functionally regulate by integrating with pathways of cell proliferation. The downregulation of miRNA molecules is involved in the evasion and inhibition of growth, thereby sustaining the signaling mechanism responsible for the cancer cell proliferation.
• Many miRNA molecules have been identified that are involved in cancer cell proliferation. For example, the miRNA-17 inhibits the expression of elongation factor 2 (E2F-1). This miRNA cluster induces the breakage of E2F-1 and makes them the functional domain. The miRNA-17 also regulates E2F-2 and E2F-3 factors. These transcription factors also cause miRNA-17 cluster’s expression, hence a feedback mechanism is maintained. Hence the miRNA-17 supports the development of many tumors and alters the feedback mechanism thereby promoting cell proliferation.
• The other example is miRNA-221, which was found to target the CDK inhibitor in glioblastoma cell types. The overexpression of these miRNA molecules increases the rate of cell proliferation and on the other hand, their down-regulation is induced by the cell cycle especially at the G1 stage. Hence, this gets arrested in cancer cell division. Some of the miRNA expression (miRNA-302, miRNA-663) also regulates certain oncogenic proteins such as p16INK4a, p27Kip1, and p21CIP1. The miRNA 663 was found to be expressed highly in nasopharyngeal carcinoma. Another miRNA molecule (miRNA-545) induces the arresting of the cell cycle in lung cancer cell types.
Role of miRNA in cancer metastasis:
• Metastasis is a complex dynamic process in cancer development. For example, in the case of EMT (epithelial-mesenchymal transition), a key step in metastasis is enhanced by the expression of E-cadherin and its associated gene activation that induces cancer cell motility and invasion.
• EMT cell invasion is regulated by TGF-beta and other important transcription factors such as SNAIL, TWIST, and ZEB. The miRNA regulated by the TGF-beta facilitates the metastasis in advanced stages in certain malignant disorders (for example miRNA-155). This molecule is over expressed and gets activated by TGF-beta, SMAD-4 signaling pathways. This miRNA molecule also induces EMT by acting on RhoA-dependent GTPases that is a key regulatory enzyme in cell polarity determination and formation of cell tight junctions, cell migration, and cancer invasion.
• On the other hand, certain miRNA molecules affect EMT that inhibits E-cadherin expression by ZEB1 and ZEB2 deactivation. The miRNA-200 transcript is suppressed by ZEB-1 AND ZEB-2 factors that form a loop of negative feedback between ZEB1 and ZEB2 and with the miRNA200 clusters. This mRNA-200 is downregulated in the cells of breast cancer along with an increase in its activity that represents mesenchymal phenotype. Hence an overexpression of miRNA-200 in E-cadherin’s mesenchymal expression induces the phenotype by increasing the rate of EMT invasion.
• The miRNA-203 is greatly suppressed due to its specific promoter’s hypermethylation in the cells of breast cancer. The restoration of miRNA-203 is brought about by the inhibition of tumor cells in lung metastasis by downregulating the SNA12 that suggests that miRNA-203 has the main role in cancer metastasis and EMT. Other miRNAs such as miRNA212, miRNA-9, and miRNA-9 are highly expressed by the activation of c-Myc proteins.
Role of miRNA in angiogenesis:
• The process of angiogenesis is an important mechanism in cancer metastasis that is achieved by the oxygen intake and absorption of more nutrients. Once the metastasis progresses, it decreases the oxygen level in neighboring tissues that leads to hypoxia in tissue cells. The hypoxia-inducible factor (HIF) is a transcription factor that is involved in the induction of many genes’ expression covering miRNA molecules too. The vascular epithelial growth factor (VEGF) is the main factor for causing angiogenesis, that is, forming new blood vessels.
• The miRNA hits HIF of the VEGF signaling mechanisms, for example, miRNA-210 gets constant during hypoxia. This molecule promotes angiogenesis both by targeting TK-eprin-A3 (tyrosine kinase) and enhances the expression of VEGF and VEGF-R2. The other miRNA molecule called miRNA-424 induces hypoxia in certain endothelial cells and increases the rate of angiogenesis.
• Another molecule miRNA-107 inhibits the HIF1beta-protein hence the miRNA-107 promoter is down-regulated, hence increase the tumor angiogenesis. The exosomal miRNA in cancer cells helps in modulating the tumor environment. The miRNA-135b is upregulated in hypoxia resistant multiple myeloma cancer cells, thereby suppressing the inhibitor of the HIF-1 signaling mechanism. Hence it is considered that the exosomal miRNA-135b may be considered as a drug target in the treatment and management of angiogenesis of multiple myelomas.
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