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miR-106a is frequently upregulated in gastric cancer and inhibits the extrinsic apoptotic pathway by targeting FAS.
- Source :
-
Molecular carcinogenesis [Mol Carcinog] 2013 Aug; Vol. 52 (8), pp. 634-46. Date of Electronic Publication: 2012 Mar 16. - Publication Year :
- 2013
-
Abstract
- 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.<br /> (Copyright © 2012 Wiley Periodicals, Inc.)
- Subjects :
- 3' Untranslated Regions
Adult
Aged
Base Pairing
Base Sequence
Cell Death genetics
Cell Line, Tumor
Humans
MicroRNAs chemistry
MicroRNAs metabolism
Middle Aged
Neoplasm Staging
Sequence Alignment
Stomach Neoplasms pathology
fas Receptor metabolism
Apoptosis genetics
Gene Expression Regulation, Neoplastic
MicroRNAs genetics
Signal Transduction
Stomach Neoplasms genetics
Stomach Neoplasms metabolism
fas Receptor genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1098-2744
- Volume :
- 52
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- Molecular carcinogenesis
- Publication Type :
- Academic Journal
- Accession number :
- 22431000
- Full Text :
- https://doi.org/10.1002/mc.21899