Published November 27, 2015 | Version v1
Journal article

MiR-506 suppresses cell proliferation and tumor growth by targeting Rho-associated protein kinase 1 in hepatocellular carcinoma

Description

Recent studies have shown that miR-506 plays important roles in human cancer progression. However, little is known about the function of miR-506 in hepatocellular carcinoma (HCC). In this study, we found that miR-506 significantly inhibits HCC cell proliferation in vitro and tumorigenicity in vivo. Moreover, miR-506 induced G1/S cell cycle arrest and apoptosis in HCC cells. Rho-associated protein kinase 1(ROCK1) was identified as a novel target of miR-506; overexpression of ROCK1 reversed the suppressive effects of miR-506 in HCC cells. Additionally, ROCK1 was found up-regulated and inversely correlated with miR-506 in HCC tissues. Therefore, our findings collectively suggest that miR-506 acts as a tumor suppressor via regulation of ROCK1 expression and may thus be a promising therapeutic target for HCC. - Highlights: • miR-506 inhibits HCC cell proliferation in vitro and tumorigenicity in vivo. • miR-506 induced G1/S cell cycle arrest and apoptosis in HCC cells. • ROCK1 was identified as a novel target of miR-506. • ROCK1 was found up-regulated and inversely correlated with miR-506 in HCC tissues.

Availability note (English)

Available from http://dx.doi.org/10.1016/j.bbrc.2015.10.043

Additional details

Identifiers

DOI
10.1016/j.bbrc.2015.10.043;
PII
S0006-291X(15)30743-9;

Publishing Information

Journal Title
Biochemical and Biophysical Research Communications
Journal Volume
467
Journal Issue
4
Journal Page Range
p. 921-927
ISSN
0006-291X
CODEN
BBRCA9

INIS

Country of Publication
United States
Country of Input or Organization
International Atomic Energy Agency (IAEA)
INIS RN
48037382
Subject category
S60: APPLIED LIFE SCIENCES;
Descriptors DEI
ANIMAL TISSUES; APOPTOSIS; CELL CYCLE; CELL PROLIFERATION; HEPATOMAS; IN VITRO; IN VIVO; PROTEINS
Descriptors DEC
BODY; CARCINOMAS; DISEASES; NEOPLASMS; ORGANIC COMPOUNDS

Optional Information

Copyright
Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.