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

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


Xiaobin Wu,1–4 Wei Liu,2–4 Xueliang Liu,5 Qing Ai,1–4 Jialin Yu1–4

1Department of Neonatology, Children’s Hospital of Chongqing Medical University, Chongqing, People’s Republic of China; 2Children’s Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, People’s Republic of China; 3Key Laboratory of Pediatrics in Chongqing, Chongqing Medical University, Chongqing, People’s Republic of China; 4Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, People’s Republic of China; 5Otolaryngology, The Chongqing Hospital of Traditional Chinese Medicine, Chongqing, People’s Republic of China

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

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