These authors contributed equally to this work.
MicroRNA-135a acts as a putative tumor suppressor by directly targeting very low density lipoprotein receptor in human gallbladder cancer
Article first published online: 27 AUG 2014
© 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Volume 105, Issue 8, pages 956–965, August 2014
How to Cite
Cancer Sci 105 (2014) 956–965
Funding Information Science and Technology Commission of Shanghai Municipality (11nm0503900). (12nm0501502). (12QA1403100). Shanghai Municipal Commission of Health and Family Planning (XYQ2011042).
- Issue published online: 27 AUG 2014
- Article first published online: 27 AUG 2014
- Accepted manuscript online: 5 JUN 2014 11:01AM EST
- Manuscript Accepted: 30 MAY 2014
- Manuscript Revised: 20 MAY 2014
- Manuscript Received: 5 FEB 2014
- Science and Technology Commission of Shanghai Municipality. Grant Numbers: 11nm0503900, 12nm0501502
- Shanghai Rising-Star Program. Grant Number: 12QA1403100
- Shanghai Municipal Commission of Health and Family Planning. Grant Number: XYQ2011042
- Gallbladder cancer;
- very low density lipoprotein receptor
The precise functions and mechanisms of microRNAs (miR) in gallbladder cancer (GBC) remain elusive. In this study, we found that miR-135a-5p expression is often dampened and correlated with neoplasm histologic grade in GBC. MicroRNA-135a-5p introduction clearly inhibited GBC cell proliferation in vitro and in vivo. Moreover, very low density lipoprotein receptor (VLDLR), which is often upregulated in GBC tissues, was identified as a direct functional target of miR-135a-5p. Furthermore, the p38 MAPK pathway was proven to be involved in miR-135a-VLDLR downstream signaling. Together, these results suggested that the miR-135a–VLDLR–p38 axis may contribute to GBC cell proliferation.