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- Title
Receptor for activated protein kinase C 1 suppresses gastric tumor progression through nuclear factor-κB pathway.
- Authors
Yong-zheng, X.; Wan-li, M.; Ji-ming, M.; Xue-qun, R.
- Abstract
OBJECTIVE: Nuclear factor-κB (NF-κB) activity is crucial for survival and proliferation of many kinds of malignancies, including gastric cancer (GC). The receptor for activated protein kinase C 1 (RACK1) is known to regulate tumor development, whereas the underlined mechanism has not been described clearly. MATERIALS AND METHODS: We analyzed expression of RACK1 in paired human GC samples by both real-time polymerase chain reaction (PCR) and western blot. Effects of RACK inhibition with small interfering RNA or its overexpression in cultured GC cell lines were evaluated in cell viabilities. NF-κB signaling was investigated using luciferase reporter assay and real-time PCR. RESULTS: RACK1 was significantly decreased in GC samples. Knockdown of RACK elevated GC cell viabilities, whereas overexpression of RACK1 suppressed tumorigenesis of GC cells. Importantly, NF-κB signaling was enhanced after RACK1 expression was inhibited, suggesting the negative regulation of the pro-oncogenic NF-κB activity by RACK1 might contribute to its tumor suppressor role in GC cells. CONCLUSION: Our results support that RACK1 suppresses gastric tumor progression through the NF-κB signaling pathway.
- Subjects
PROTEIN kinase regulation; GASTRIC diseases; CANCER invasiveness; PROTEIN kinase genetics; PHOSPHOTRANSFERASES; GENETICS
- Publication
Indian Journal of Cancer, 2015, Vol 52, pe172
- ISSN
0019-509X
- Publication type
Article
- DOI
10.4103/0019-509X.186572