miR-106a is frequently upregulated in gastric cancer and inhibits the extrinsic apoptotic pathway by targeting FAS
Article first published online: 16 MAR 2012
Copyright © 2012 Wiley Periodicals, Inc.
Volume 52, Issue 8, pages 634–646, August 2013
How to Cite
Wang, Z., Liu, M., Zhu, H., Zhang, W., He, S., Hu, C., Quan, L., Bai, J. and Xu, N. (2013), miR-106a is frequently upregulated in gastric cancer and inhibits the extrinsic apoptotic pathway by targeting FAS. Mol. Carcinog., 52: 634–646. doi: 10.1002/mc.21899
- Issue published online: 12 JUL 2013
- Article first published online: 16 MAR 2012
- Manuscript Accepted: 14 FEB 2012
- Manuscript Revised: 3 FEB 2012
- Manuscript Received: 9 NOV 2011
- National Natural Science Foundation. Grant Numbers: 39925020, 81021061
- National Basic Research Program, P. R. China. Grant Number: 2011CB910700
- gastric cancer;
Emerging evidence has shown the association of aberrantly expressed miR-106a with cancer development, however, little is known about its potential role in gastric carcinogenesis. In our present study, obviously overexpressed miR-106a was found in gastric cancer tissues compared with their nontumor counterparts. Suppression of miR-106a significantly inhibited gastric cancer cell proliferation and triggered apoptosis. Bioinformatic analysis combining with validation experiments identified FAS as a direct target of miR-106a. Rescue experiments and examination of caspase-8, PARP and caspase-3 further approved that miR-106a could inhibit gastric cancer cell apoptosis through interfering with FAS-mediated apoptotic pathway. Moreover, a significant inverse correlation was found between miR-106a and FAS expression not only in gastric cancer cell lines but also in gastric cancer specimens. Taken together, these findings suggest that ectopicly overexpressed miR-106a may play an oncogenic role in gastric carcinogenesis and impair extrinsic apoptotic pathway through targeting FAS. © 2012 Wiley Periodicals, Inc.