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SIRT4 acts as a tumor suppressor in gastric cancer by inhibiting cell proliferation, migration, and invasion

Authors Sun H, Huang D, Liu G, Jian F, Zhu J, Zhang L

Received 5 November 2017

Accepted for publication 23 January 2018

Published 10 July 2018 Volume 2018:11 Pages 3959—3968

DOI https://doi.org/10.2147/OTT.S156143

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yao Dai


Hongjie Sun,1 Dongli Huang,1 Guozheng Liu,1 Fengguo Jian,1 Jianfang Zhu,1 Lixia Zhang2

1Department of General Surgery, Changyi People’s Hospital, Changyi, Shandong, People’s Republic of China; 2Department of Nuclear Medicine, Zhejiang Provincial Hospital of Traditional Chinese Medicine (The First Affiliated Hospital of Zhejiang Chinese Medical University), Hangzhou, Zhejiang, People’s Republic of China

Background: Previous study has proven that SIRT4 is downregulated in gastric cancer (GC), but the role of SIRT4 has not been clearly understood. The aim of our work was to explore in detail the function and mechanism of SIRT4 in GC.
Methods: A total of 86 pairs of GC tumor tissues and adjacent normal tissues were collected, and quantitative real-time polymerase chain reaction and Western blotting analyses were used to determine the expression of SIRT4.
Results: Our study revealed that the expression of SIRT4 was downregulated in GC tissues and cells. In addition, the low expression of SIRT4 was negatively correlated with tumor size, pathological grade, and lymph node metastasis, which predicted a poor prognosis. Multiple functional experiments, including Cell Counting Kit-8 assay as well as colony formation assay, demonstrated SIRT4 suppressed cell proliferation. Moreover, we found epithelial–mesenchymal transition was regulated by SIRT4, thereby regulating cell migration and invasion.
Conclusion: Overall, our findings show that SIRT4 serves as a tumor suppressor in GC and might act as a novel biomarker and a therapeutic target of GC.

Keywords: sirtuin 4, proliferation, migration, invasion, epithelial–mesenchymal transition, EMT

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