<p>MicroRNA-181c suppresses growth and metastasis of hepatocellular carcinoma by modulating NCAPG</p>

Abstract

Purpose: Numerous studies have shown that the expression of microRNA-181c (miR-181c) is inhibited in various cancers, which suggests that it has a cancer suppressive effect. In the current study, we evaluated the regulation and characteristics of miR-181c in human hepatocellular carcinoma (HCC). Materials and methods: Samples of tumor tissues and adjacent non-tumor tissues were collected from 52 patients with HCC, and expression levels of miR-181c in these samples were investigated via quantitative real-time polymerase chain reaction. HCC cell migration and invasion were investigated via wound healing assays and transwell assays. HCC cell apoptosis rates were assessed via flow cytometry, and HCC proliferation was assessed via 5-ethynyl-20-deoxyuridine assays. In vivo tumors were initiated by subcutaneously inoculating HCC cells into nude mice. And various biomarkers were investigated via western blotting. Results: In microarray datasets and tumor tissues, significant downregulation of miR-181c was apparent compared with non-tumorous adjacent tissues. Expression of miR-181c in HCC cells was also significantly lower than it was in normal human liver cells. miR-181c regulated the migration, invasion, apoptosis, and proliferation of HCC cell lines in vitro, and tumor development in vivo. Observations also suggest that miR-181c regulates NCAPG in HCC cells, and its expression affects cellular invasion, migration, proliferation, and apoptosis. There was a negative correlation between miR-181c expression and NCAPG in HCC tissue samples. Conclusion: miR-181c exhibits tumor-suppression via the regulation of NCAPG levels.

NCAPG upregulation mediated by four microRNAs combined with activation of the p53 signaling pathway is a predictor of poor prognosis in patients with breast cancer

“…NCAPG is a subunit of the condensin complex and is hypothesized to serve important roles in the mitosis and meiosis responsible for the condensation and stabilization of chromosomes ( 16 ). Several studies have revealed that higher expression levels of NCAPG serve a role in cell proliferation, angiogenesis and tumor therapy resistance in cancer ( 22 , 58 , 59 ). Wang et al ( 22 ) revealed that transient inhibition of NCAPG using specific siRNAs resulted in a significant decrease in cell proliferation and migration in vitro in hepatocellular carcinoma.…”

“…Wang et al ( 22 ) revealed that transient inhibition of NCAPG using specific siRNAs resulted in a significant decrease in cell proliferation and migration in vitro in hepatocellular carcinoma. Ai et al ( 59 ) reported that miR-181c induced hepatocellular carcinoma suppression via the regulation of NCAPG expression. However, at present, the specific mechanism by which NCAPG exerts its effects in cancer remains unclear.…”

miRNAs expression signature potentially associated with lymphatic dissemination in locally advanced prostate cancer

“…Significant downregulation of miR-181c was also detected in the case of hepatocellular carcinoma when compared with normal tissues. miR-181c regulated migration, invasion, apoptosis, and proliferation of hepatocellular carcinoma cell lines in vitro and tumor development in vivo [78].…”

MiR-181c-5p Promotes Inflammatory Response during Hypoxia/Reoxygenation Injury by Downregulating Protein Tyrosine Phosphatase Nonreceptor Type 4 in H9C2 Cardiomyocytes

“…The miR-181 family (including miR-181a, miR-181b, miR-181c, and miR-181d) plays diverse roles in regulating various cellular and biological processes through posttranscriptional regulation of target genes [8][9][10][11][12]. Accumulating evidence suggests a central role for the miR-181 family in inflammation by regulating target proteins invovled in critical inflammatory signalling pathways, such as NFκB signalling [13,14].…”