Oncotarget

Research Papers:

TES inhibits colorectal cancer progression through activation of p38

Huili Li _, Kun Huang, Lu Gao, Lixia Wang, Yanfeng Niu, Hongli Liu, Zheng Wang, Lin Wang, Guobin Wang and Jiliang Wang

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Oncotarget. 2016; 7:45819-45836. https://doi.org/10.18632/oncotarget.9961

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Abstract

Huili Li1,*, Kun Huang2,*, Lu Gao3, Lixia Wang4, Yanfeng Niu1, Hongli Liu5, Zheng Wang1,6, Lin Wang6, Guobin Wang1, Jiliang Wang1

1Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

2Institution of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

3Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China

4Department of Radiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

5Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

6Research Center for Tissue Engineering and Regenerative Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

*These authors have contributed equally to this work

Correspondence to:

Lin Wang, email: lin_wang@hust.edu.cn

Guobin Wang, email: wangguobin68@126.com

Jiliang Wang, email: jiliang_wang@hust.edu.cn

Keywords: TESTIN gene, tumor suppressor gene, colorectal cancer, HCT116 cell and DLD-1 cell, p38 MAP kinase

Received: June 24, 2015    Accepted: May 29, 2016    Published: June 13, 2016

ABSTRACT

The human TESTIN (TES) gene has been identified as a candidate tumor suppressor based on its location at a common fragile site – a region where loss of heterozygosity has been detected in numerous types of tumors. To investigate its role in colorectal cancer (CRC), we examined TES protein levels in CRC tissue samples and cell lines. We observed that TES was markedly reduced in both CRC tissue and cell lines. Additionally, overexpression of TES significantly inhibited cell proliferation, migration, and invasion, while increasing cell apoptosis in colon cancer cells. By contrast, shRNA-mediated TES knockdown elicited the opposite effects. TES inhibited the progression of CRC by up-regulating pro-apoptotic proteins, down-regulating anti-apoptotic proteins, and simultaneously activating p38 mitogen-activated protein kinase (MAPK) signaling pathways. Collectively, these data indicate that TES functions as a necessary suppressor of CRC progression by activating p38-MAPK signaling pathways. This suggests that TES may have a potential application in CRC diagnosis and targeted gene therapy.


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