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 ORIGINAL ARTICLE
Year : 2015  |  Volume : 52  |  Issue : 7  |  Page : 172-175

Receptor for activated protein kinase C 1 suppresses gastric tumor progression through nuclear factor-kB pathway


Department of General Surgery, Huaihe Hospital of Henan University, Kaifeng 475000, Henan Province, PR China

Correspondence Address:
R Xue-qun
Department of General Surgery, Huaihe Hospital of Henan University, Kaifeng 475000, Henan Province
PR China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-509X.186572

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OBJECTIVE: Nuclear factor-kB (NF-kB) 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-kB 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-kB signaling was enhanced after RACK1 expression was inhibited, suggesting the negative regulation of the pro-oncogenic NF-kB 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-kB signaling pathway.






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