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TRIM37 targets AKT in the growth of lung cancer cells

Authors Dong SM, Pang XQ, Sun HJ, Yuan CL, Mu CY, Zheng S

Received 9 August 2018

Accepted for publication 12 October 2018

Published 8 November 2018 Volume 2018:11 Pages 7935—7945

DOI https://doi.org/10.2147/OTT.S183303

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Andrew Yee

Peer reviewer comments 2

Editor who approved publication: Dr Takuya Aoki


Shumin Dong,1 Xueqin Pang,2 Haijun Sun,3 Chunluan Yuan,4 Chuanyong Mu,5 Shiying Zheng6

1Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, The First People’s Hospital of Lianyungang City, Lianyungang, Jiangsu 222000, People’s Republic of China; 2Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, People’s Republic of China; 3Department of Thoracic Surgery, The First People’s Hospital of Lianyungang City, Lianyungang, Jiangsu 222000, People’s Republic of China; 4Department of Oncology, The First People’s Hospital of Lianyungang City, Lianyungang, Jiangsu 222000, People’s Republic of China; 5Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, People’s Republic of China; 6Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, People’s Republic of China

Background: TRIM37 is an ubiquitin E3 ligase. Growing evidence has demonstrated the high value of TRIM37 as a potential biomarker for diagnosis of certain cancers. However, the biological function of TRIM37 in lung cancer is still unknown.
Materials and methods: In order to gain a deep insight into the function of TRIM37 in lung cancer cells, in the present study lentiviral vector was used to mediate RNA interference and overexpression of TRIM37 in lung cancer cells (H292, H358, and H1299). In addition, a specific AKT inhibitor LY294002 was utilized to examine the correlation between the expression of TRIM37 and AKT.
Results: TRIM37 acts as a positive regulator of cell proliferation in lung cancer cells. Moreover, cell apoptosis analyses showed the antiapoptosis function of TRIM37, which was mainly dependent on the regulation of BCL2 and BAX. Our results also indicated that AKT might be a target of TRIM37 in lung cancer cells.
Conclusion: This research not only helps in understanding the molecular mechanisms of TRIM37 in detail but also provides evidence to develop novel biomarkers for lung cancer diagnosis.

Keywords: TRIM37, cell proliferation, apoptosis, BCL2, BAX, AKT

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