miR-493-5p suppresses hepatocellular carcinoma cell proliferation through targeting GP73.

Biomed Pharmacother

Department of Gastroenterology and Clinical Laboratory, Nantong Third Hospital Affiliated to Nantong University, Jiangsu, 226006, China. Electronic address:

Published: June 2017

Aberrant expression of miRNAs has been documented to play critical roles in the development and progression of hepatocellular carcinoma (HCC). However, the expression pattern, functional roles and regulatory mechanism of miR-493-5p in HCC have not been addressed. Herein, we found that miR-493-5p was significantly downregulated in HCC tissues and was tightly associated with tumor size, tumor differentiation grade and TNM stage of HCC patients. Overexpression of miR-493-5p inhibited HCC cell proliferation, arrested cell cycle in G0/G1 phase and induced cell apoptosis. Bioinformatical analysis and luciferase reporter assay further proved that Golgiprotein73 (GP73), an oncogene which was generally overexpressed in HCC, acted as a novel target of miR-493-5p. MiR-493-5p could inhibit GP73 both mRNA and protein expression. Moreover, overexpression of GP73 could reverse the inhibitory effects of miR-493-5p mediated HCC cell proliferation. In addition, upregulated GP73 in HCC tissues was inversely correlated with the miR-493-5p expression levels in the HCC tissues. Collectively, our present study demonstrates that miR-493-5p is downregulated in HCC and it can suppress the proliferation of HCC cells, partly at least, via directly targeting GP73. Besides, this study provides a novel insight into the mechanism of hepatocarcinogenesis and a promising blueprint for miR-493-5p-GP73 axis-oriented treatment of HCC.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.biopha.2017.04.029DOI Listing

Publication Analysis

Top Keywords

cell proliferation
12
hcc
12
hcc tissues
12
mir-493-5p
9
hepatocellular carcinoma
8
targeting gp73
8
mir-493-5p downregulated
8
downregulated hcc
8
hcc cell
8
gp73
6

Similar Publications

Aging is accompanied by a decline in neovascularization potential and increased susceptibility to ischemic injury. Here, we confirm the age-related impaired neovascularization following ischemic leg injury and impaired angiogenesis. The age-related deficits in angiogenesis arose primarily from diminished EC proliferation capacity, but not migration or VEGF sensitivity.

View Article and Find Full Text PDF

The Effects of Nitric Oxide on Choroidal Gene Expression.

J Bioinform Syst Biol

January 2024

Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, 73104, United States.

Purpose: Nitric oxide (NO) is recognized as an important biological mediator that controls several physiological functions, and evidence is now emerging that this molecule may play a significant role in the postnatal control of ocular growth and myopia development. We therefore sought to understand the role that nitric oxide plays in visually-guided ocular growth in order to gain insight into the underlying mechanisms of this process.

Methods: Choroids were incubated in organ culture in the presence of the NO donor, PAPA- NONOate (1.

View Article and Find Full Text PDF

Background: The Arp2/3 complex is a key regulator of tumor metastasis, and targeting its subunits offers potential for anti-metastatic therapy. However, the expression profiles, prognostic relevance, and diagnostic value of its subunits across cancers remain poorly understood. This study aims to investigate the clinical relevance of Arp2/3 complex subunits, particularly ARPC1A, in pan-cancer, and to further analyze the potential biological mechanisms of ARPC1A, as well as its association with immune infiltration and chemotherapy drug sensitivity.

View Article and Find Full Text PDF

Introduction: Breast cancer (BC) is the most prevalent malignant tumor in women, with triple-negative breast cancer (TNBC) showing the poorest prognosis among all subtypes. Glycosylation is increasingly recognized as a critical biomarker in the tumor microenvironment, particularly in BC. However, the glycosylation-related genes associated with TNBC have not yet been defined.

View Article and Find Full Text PDF

Introduction: Macrophages exhibit marked phenotypic heterogeneity within and across disease states, with lipid metabolic reprogramming contributing to macrophage activation and heterogeneity. Chronic inflammation has been observed in human benign prostatic hyperplasia (BPH) tissues, however macrophage activation states and their contributions to this hyperplastic disease have not been defined. We postulated that a shift in macrophage phenotypes with increasing prostate size could involve metabolic alterations resulting in prostatic epithelial or stromal hyperplasia.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!