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Overexpression of MCPH1 inhibits the migration and invasion of lung cancer cells.

OncoTargets and therapy (2018-06-07)
Xiaobin Wu, Wei Liu, Xueliang Liu, Qing Ai, Jialin Yu
ZUSAMMENFASSUNG

The role of dysfunction of MCPH1, a recently identified tumor suppressor gene, has not yet been established in lung cancer. In our previous study, it was reported that MCPH1 expression is downregulated in lung cancer tissues and that MCPH1 overexpression inhibits the proliferation of non-small-cell lung cancer cells. The results can be found in the APJC and Oncology Letters journals. Kaplan-Meier survival analysis was conducted to explore the prognostic significance of MCPH1. Cell experiments were performed to investigate the effects of MCPH1 on the biologic behaviors of lung cancer cells. In the current study, microarray analysis of MCPH1 revealed that lung cancer patients with high MCPH1 expression had longer relapse-free survival. Overexpression of MCPH1 in A549 lung carcinoma cells successfully inhibited cell migration and invasion. Moreover, overexpression of MCPH1 inhibited migration and invasion by regulating the activities of several proteins that control the epithelial-mesenchymal transition, such as Slug, Snail, E-cadherin, Mdm2, and p53. Our results indicate that downregulation of MCPH1 correlates with tumor progression in lung cancer, and hence MCPH1 may be an important tumor suppressor gene and a novel candidate therapeutic target in lung cancer.

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Sigma-Aldrich
Anti-MDM2 antibody ,Mouse monoclonal, clone HDM2-323, purified from hybridoma cell culture
Sigma-Aldrich
ANTI-P53 (S15) antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution