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Receptor for activated protein kinase C 1 suppresses gastric tumor progression through nuclear factor‑κB pathway.
Indian J Cancer ; 2015 Dec; 52(7)Suppl_3: s172-s175
Article in English | IMSEAR | ID: sea-176764
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.

Full text: Available Index: IMSEAR (South-East Asia) Language: English Journal: Indian J Cancer Year: 2015 Type: Article

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Full text: Available Index: IMSEAR (South-East Asia) Language: English Journal: Indian J Cancer Year: 2015 Type: Article