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ATG7 promotes the tumorigenesis of lung cancer but might be dispensable for prognosis predication: a clinicopathologic study

Authors Sun S, Wang Z, Tang F, Hu P, Yang Z, Xue C, Gong J, Shi L, Xie C

Received 5 March 2016

Accepted for publication 15 June 2016

Published 11 August 2016 Volume 2016:9 Pages 4975—4981


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Debarshi Roy

Peer reviewer comments 2

Editor who approved publication: Dr William Cho

Shaoxing Sun,1,2,* Zhihao Wang,1,2,* Fang Tang,1,2 Pengchao Hu,3 Zetian Yang,4 Chao Xue,4 Jun Gong,1,2 Liu Shi,1,2 Conghua Xie,1,2

1Department of Radiation and Medical Oncology, 2Hubei Key Laboratory of Tumor Biological Behaviors, Zhongnan Hospital of Wuhan University, 3Department of Pathology and Pathophysiology, School of Basic Medical Sciences, Wuhan University, 4Department of Thoracic and Cardiovascular Surgery, Zhongnan Hospital of Wuhan University, Wuhan, People’s Republic of China

*These authors contributed equally to this work

Abstract: Lung cancer is the most frequent cause of cancer-related death worldwide. Dysregulated autophagy is often observed in lung cancer. Autophagy-related 7 (ATG7) is an autophagy gene that is essential for the biogenesis of autophagosomes. Although ATG7-deficient mouse models have demonstrated that ATG7-dependent autophagy is required for lung cancer tumorigenesis, the relationship between ATG7 expression levels and human lung cancer is unclear. Here, we demonstrate that ATG7 was overexpressed in human lung cancer tissues compared with normal tissues. However, ATG7 expression was not associated with tumor differentiation, tumor size, or TNM stage. Moreover, the overexpression of ATG7 did not influence the overall survival of the lung cancer patients. Therefore, our results indicate that ATG7 might be dispensable for tumor growth and chemotherapy efficacy in human lung cancer.

Keywords: ATG7, autophagy, lung cancer, prognosis, clinicopathologic study

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