MiR-506 suppresses cell proliferation and tumor growth by targeting Rho-associated protein kinase 1 in hepatocellular carcinoma
Creators
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.2015.10.043Additional 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.