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MEK/ERK pathway-mediated GCIP expression involved in metastases of lung adenocarcinoma.
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|摘要:||GCIP (Grap2 and Cyclin D Interacting Protein) is identified in yeast two hybrid screening using the Grap2 and Cyclin D1 as baits. Previously studies have shown that overexpression of GCIP reduced phosphorylation of RB and inhibited E2F1-mediated transcriptional activity. In colon cancer and breast cancer cell lines, ectopic expression of GCIP resulted in a significant inhibition on anchorage- independent growth. Further examination of GCIP protein level in tumors indicated that GCIP scores of breast carcinomas were significantly correlated with tumor histological grade and clinical outcome. In this study we investigated the expression and the biological function of GCIP in human lung adenocarcinoma cells. Our data showed that GCIP expression in CL1-5 cells, which exhibit a relative higher invasive ability as compared with its parental cells CL1-0, was significant lower than that in CL1-0 cells. Interestingly, the level of phosphorylated ERK in CL1-5 was higher than that in CL1-0 cells. U0126 treatment resulted in the increase of GCIP protein expression but not mRNA level in CL1-5 cells. Furthermore, the protein stability of GCIP in CL1-5 was also lower than that in CL1-0. It's likely that the lower protein stability of GCIP may result in the lower level of GCIP in CL1-5. To gain better understanding of the GCIP function in human lung adenocarcinoma, overexpression of GCIP reduced the invasive ability in CL1-5 cells. In contrast, knockdown of GCIP expression by siRNA in poorly invasive CL1-0 cell line enhanced its invasive ability. Taken together, these results indicate that GCIP play a critical role in anti-invasiveness and MEK/ERK signal pathway may control GCIP expression in human lung adenocarcinoma.|
|Appears in Collections:||生物醫學研究所|
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