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Authors Wu X, Liu W, Liu X, Ai Q, Yu J
Received 5 November 2017
Accepted for publication 19 March 2018
Published 25 May 2018 Volume 2018:11 Pages 3111—3117
DOI https://doi.org/10.2147/OTT.S156102
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 2
Editor who approved publication: Dr Samir Farghaly
Background: 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.
Methods: 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.
Results: 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.
Conclusion: 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.
Keywords: MCPH1, migration, invasion, p53, lung cancer, Mdm2