Overexpression of APC11 predicts worse survival in lung adenocarcinoma
Authors Zhou J, Zhang S, Fu G, He Z, Xu Y, Ye W, Chen Z
Received 14 June 2018
Accepted for publication 3 September 2018
Published 17 October 2018 Volume 2018:11 Pages 7125—7132
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Yao Dai
Jiayu Zhou,1,* Shizhen Zhang,2,* Guoxiang Fu,3 Zhengfu He,1 Yong Xu,1 Weiwen Ye,1 Zhoumiao Chen1
1Department of Thoracic Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, Zhejiang Province, China; 2Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310029, Zhejiang Province, China; 3Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, Zhejiang Province, China
*These authors contributed equally to this work
Background: Anaphase-promoting complex subunit 11 (APC11) plays an important role in gathering E2 and catalyzing ubiquitin-chain formation to support ubiquitination of substrates by acting as a catalytic core subunit of anaphase-promoting complex (APC/C). However, whether APC11 is implicated in the tumorigenesis of lung cancer is never known.
Materials and methods: In this study, we used an online survival analysis software to estimate the prognostic value of APC11 mRNA expression level for lung cancer. Cell Counting Kit-8 assay, colony-forming assay, and transwell assay were used to assess the biological functions of APC11 in lung cancer cells. Then, 107 lung cancer patient tissues were collected to examine the expression level of APC11 by immunohistochemistry staining. Kaplan–Meier method and univariate Cox regression analysis were performed to reveal the prognostic value of APC11 protein expression in lung cancer.
Results: Higher mRNA level of APC11 was significantly associated with worse survival for lung adenocarcinoma, but not for lung squamous cell carcinoma. Knockdown of APC11 by siRNA apparently inhibited cell proliferation and colon formation in both H1299 and H358 cells. In addition, silencing of APC11 decreased cell migrative and invasive abilities. Moreover, immunohistochemical analysis showed that APC11 was highly expressed in lung cancer tissues, and multivariate analysis suggested that APC11 overexpression was an independent prognostic factor in lung adenocarcinoma.
Conclusion: We suggest that APC11 could serve as a prognostic biomarker and a novel target in treating lung adenocarcinoma.
Keywords: APC11, lung cancer, cell proliferation, migration, invasion
Corrigendum for this paper has been published.
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