Restoration of miR-20a expression suppresses cell proliferation, migration, and invasion in HepG2 cells

Abstract

ObjectiveTo study microRNA (miR)-20a expression in hepatocellular carcinoma (HCC) and its effects on the proliferation, migration, and invasion of HepG2.MethodsThe real-time polymerase chain reaction was used to detect the expression of miR-20a in HCC tissue and normal tissue, as well as in HCC cell lines and normal liver cells. miR-20a mimic and miR negative control (NC) were transfected into HepG2 cells. MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) assay was used to detect cell proliferation. Annexin fluorescein isothiocyanate/propidium iodide assay was run to examine the early apoptosis of cells. Transwell chamber assay was carried out to investigate the cell invasion and migration abilities.ResultsmiR-20a was lowly expressed both in HCC tissues and HCC cell lines. After transfection of exogenous miR-20 mimics, miR-20a expression in HepG2 cells was significantly increased by 61.29% compared to the blank group (P<0.01). MTT assay showed that the growth of HepG2 cells in the miR-20a mimics group was significantly inhibited, and optical density values during the 36–96 hour time period were dramatically decreased compared to the blank group (P<0.01). Apoptosis rates of the miR-20a mimics group were higher than those of the blank and NC groups (both P<0.01). The number of HCC cells after transfection by miR-20a mimics in the G1 and S phases were 15.88% and 7.89%, respectively, which were lower than in the blank and NC groups (both P<0.05). Transwell assay showed that in the miR-20a mimics group the number of cell migration and invasion were 0.459 and 0.501 times that of the blank group (both P<0.01), and the migration and inhibition rates were 54.1% and 51.4%, respectively. After closing target gene CCND1 in HepG2 cells, the number of cell migration and invasion in the small interfering (si)-CCND1 group were 0.444 and 0.435 times that of the si-NC group (P<0.05); and compared to the si-NC group, the migration and inhibition rates were 55.6% and 56.5%, respectively.ConclusionmiR-20a can inhibit the growth, invasion, and migration of HepG2 cells, and is therefore promising as a new molecular target for diagnosis and therapy of HCC.

Upregulation of miR-129-5p increases the sensitivity to Taxol through inhibiting HMGB1-mediated cell autophagy in breast cancer MCF-7 cells

“…However, some patients still have lower Taxol sensitivity because of drug resistance, which leads to poor prognosis of patients (8). Recently, altered levels of autophagy and miRNAs were attractive candidates for study as regulators of chemosensitivity in breast cancer (11,16,26). In the present study, we found that miR-129-5p increased the Taxol-induced apoptosis while inhibiting autophagy.…”

“…Micro RNAs (miRNAs) are a class of short, endogenous, non-coding RNAs (∼20–24 nucleotides) that regulate the expression of a diversity of genes (10). They have been identified to be involved in a variety of biological processes (11 –13). Recently, an increasing number of studies have reported that dysregulation of miRNAs might be related to drug resistance (14 –16).…”

An Overview of miRNAs Involved in PASMC Phenotypic Switching in Pulmonary Hypertension

“…miR-20a: the dysregulation of miR-20a expression is involved in the development of a variety of cancers [ 113 ]. In PH, miR-20a targets PKG1, promotes the activation of Elk-1, and competes for the binding sites of MYOCD and SRF, eventually leading to the dissociation of the MYOCD-SRF complex and termination of the SM-specific gene expression programme.…”