MicroRNA 320, an Anti-Oncogene Target miRNA for Cancer Therapy

Abstract

MicroRNAs are a set of highly conserved non-coding RNAs that control gene expression at the post-transcriptional/translational levels by binding to the 3′-UTR of diverse target genes. Increasing evidence indicates that miRNAs not only play a vital role in many biological processes, but they are also frequently deregulated in pathological conditions, including cancer. The miR-320 family is one of many tumor suppressor families and is composed of five members, which has been demonstrated to be related to the repression of epithelial-mesenchymal transition (EMT) inhibition, cell proliferation, and apoptosis. Moreover, this family has been shown to regulate drug resistance, and act as a potential biomarker for the diagnosis, prognosis, and prediction of cancer. In this review, we summarized recent research with reference to the tumor suppressor function of miR-320 and the regulation mechanisms of miR-320 expression. The collected evidence shown here supports that miR-320 may act as a novel biomarker for cancer prognosis and therapeutic response to cancer treatment.

MiR-320-3p Regulates the Proliferation and Differentiation of Myogenic Progenitor Cells by Modulating Actin Remodeling

“…Previous studies have shown the dysregulation of miR-320-3p in various malignancies and its diverse role on cell proliferation and cell cycle. MiR-320-3p frequently appears to function as a tumor suppressor by inhibiting proliferation, invasion, and migration [ 14 ]. In contrast, several studies have demonstrated that miR-320-3p increases proliferation and promotes cell cycle progression in various cells.…”

“…MiR-320-3p is a member of the miR-320 family (miR-320a/-b/-c/-d/-e) and is the most widely distributed in all primates [ 13 ]. Since the miR-320 family plays a multifaceted role in cell proliferation, apoptosis, and metastasis, previous studies have mainly focused on the significance of miR-320-3p on oncogenesis and cancer progression [ 14 ]. Nevertheless, in addition to the relation to obesity and metabolic diseases [ 12 ], miR-320-3p has been linked to several conditions resulting in muscle wasting, such as oxidative stress, ER stress, mitochondrial dysfunction, apoptosis, and enhanced autophagy [ 14 , 15 , 16 , 17 , 18 ].…”

“…Since the miR-320 family plays a multifaceted role in cell proliferation, apoptosis, and metastasis, previous studies have mainly focused on the significance of miR-320-3p on oncogenesis and cancer progression [ 14 ]. Nevertheless, in addition to the relation to obesity and metabolic diseases [ 12 ], miR-320-3p has been linked to several conditions resulting in muscle wasting, such as oxidative stress, ER stress, mitochondrial dysfunction, apoptosis, and enhanced autophagy [ 14 , 15 , 16 , 17 , 18 ]. Hence, these findings imply that miR-320-3p may be implicated in myogenesis and muscle homeostasis by regulating cell proliferation, differentiation, and regeneration.…”

MicroRNAs and Stem-like Properties: The Complex Regulation Underlying Stemness Maintenance and Cancer Development

“…Tumor-suppressor miRNA downregulated in breast cancer, glioma, gastric cancer, retinoblastoma, and human non-small-cell lung cancer. It is mainly involved in the inhibition of EMT, reducing the levels of E-Cadherin and increasing that of N-Cadherin and Vimentin [72][73][74][75][76][77][78].…”

“…These miRNAs bind the 3′-UTR region of the cell-cycle inhibitors p57 and p21, unlocking the cells from the G1 cellcycle arrest [70]. In cancer cells, miR-320 has a tumor-suppressor function; it is downregulated in different cancers such as breast cancer, glioma, gastric cancer, retinoblastoma, and human non-small-cell lung cancer, and it represents an important EMT inhibitor by reducing the levels of E-Cadherin and increasing those of N-Cadherin and Vimentin [31,72,[75][76][77][78]. MiR-30 is one of the four miRNAs able to repress the expression of LIN28 protein in both ESCs (mouse embryonic stem cell lines R1 and C57BL/6J-693, ATCC and The Jackson Laboratory) and LIN28-positive human breast cancer cell line T47D, directly binding its 3′-UTR.…”