期刊
ONCOLOGY RESEARCH AND TREATMENT
卷 38, 期 7-8, 页码 362-366出版社
KARGER
DOI: 10.1159/000433499
关键词
Gastric cancer; GAS5; Cell cycle; CDK6
类别
资金
- Jiangsu Provincial ministry of health [H201347]
- 333 projects of Jiangsu province [CAE01101-07]
Introduction: As it is not clear whether growth arrest-specific 5 (GAS5) inhibits gastric cancer (GC) cell proliferation by regulating cell cycle, we analyzed the effect of GAS5 on cell cycle regulation of GC cells and explored the underlying mechanism. Methods: We measured GAS5 levels in GC tissues and corresponding normal tissues, and analyzed the role of GAS5 in regulation of cell proliferation and cell cycle in GC cells using CCK-8 assay and flow cytometry. We also measured the expression of P21 and CDK6 proteins after transfection of AGS and MGC-803 cells with pLJM-GAS5 and GAS5 siRNA, respectively, by western blotting. Results: GAS5 expression was significantly lower in GC tissues relative to normal tissues, and its lower expression was correlated with larger tumor size and a more advanced clinical stage of GC. GAS5 induced growth arrest of GC cells through inhibition of G1-S phase translation. The action of GAS5 may be mediated by upregulation of P21 and suppression of CDK6. Conclusion: These data enhance our understanding of the important role that GAS5 plays in the molecular etiology of GC and suggest a potential of GAS5 as a new therapeutic target for GC treatment. (C) 2015 S. Karger GmbH, Freiburg
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