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- W2894619384 abstract "The p53‐inducible gene 3 ( PIG 3) is one of the p53‐induced genes at the onset of apoptosis, which plays an important role in cell apoptosis and DNA damage response. Our previous study reported an oncogenic role of PIG 3 associated with tumor progression and metastasis in non‐small cell lung cancer ( NSCLC ). In this study, we further analyzed PIG 3 mRNA expression in 504 lung adenocarcinoma ( LUAD ) and 501 lung squamous cell carcinoma ( LUSC ) tissues from The Cancer Genome Atlas database and we found that PIG 3 expression was significantly higher in LUAD with lymph node metastasis than those without, while no difference was observed between samples with and without lymph node metastasis in LUSC . Gain and loss of function experiments were performed to confirm the metastatic role of PIG 3 in vitro and to explore the mechanism involved in its oncogenic role in NSCLC metastasis. The results showed that PIG 3 knockdown significantly inhibited the migration and invasion ability of NSCLC cells, and decreased paxillin, phospho‐focal adhesion kinase ( FAK ) and phospho‐Src kinase expression, while its overexpression resulted in the opposite effects. Blocking FAK with its inhibitor reverses PIG 3 overexpression‐induced cell motility in NSCLC cells, indicating that PIG 3 increased cell metastasis through the FAK /Src/paxillin pathway. Furthermore, PIG 3 silencing sensitized NSCLC cells to FAK inhibitor. In conclusion, our data revealed a role for PIG 3 in inducing LUAD metastasis, and its role as a new FAK regulator, suggesting that it could be considered as a novel prognostic biomarker or therapeutic target in the treatment of LUAD metastasis." @default.
- W2894619384 created "2018-10-12" @default.
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- W2894619384 date "2018-10-26" @default.
- W2894619384 modified "2023-10-16" @default.
- W2894619384 title "p53‐inducible gene 3 promotes cell migration and invasion by activating the<scp>FAK</scp>/Src pathway in lung adenocarcinoma" @default.
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- W2894619384 doi "https://doi.org/10.1111/cas.13818" @default.
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