Oncotarget

Research Papers:

Up-regulation of CIT promotes the growth of colon cancer cells

Zehua Wu, Xiangying Zhu, Wendi Xu, Yu Zhang, Lin Chen, Fabo Qiu, Binyuan Zhang, Liqun Wu, Zhihai Peng and Huamei Tang _

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Oncotarget. 2017; 8:71954-71964. https://doi.org/10.18632/oncotarget.18615

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Abstract

Zehua Wu1,*, Xiangying Zhu2,3,*, Wendi Xu4, Yu Zhang5, Lin Chen3, Fabo Qiu1, Binyuan Zhang1, Liqun Wu1, Zhihai Peng2 and Huamei Tang5

1Department of Hepatobiliary Surgery, The Affiliated Hospital of Qingdao University, Qingdao 266003, People’s Republic of China

2Department of General Surgery, Shanghai Jiaotong University Affiliated First People’s Hospital, Shanghai 200080, People’s Republic of China

3R & D Department, Shanghai GeneChem Limited Company, Shanghai 201203, People’s Republic of China

4Department of Continuing Medical Education, The Affiliated Hospital of Qingdao University, Qingdao 266003, People’s Republic of China

5Department of Pathology, Shanghai Jiaotong University Affiliated First People’s Hospital, Shanghai 200080, People’s Republic of China

*These authors have contributed equally to this work

Correspondence to:

Huamei Tang, email: [email protected]

Zhihai Peng, email: [email protected]

Keywords: CIT, colon cancer, cell growth, apoptosis, p53

Received: July 18, 2016     Accepted: May 06, 2017     Published: June 27, 2017

ABSTRACT

Colon cancer is one of the major causes of cancer mortality worldwide. However, the underlying mechanism and therapeutic targets of colon cancer have not yet been fully elucidated. In the present study, we demonstrate that citron rho-interacting, serine/threonine kinase 21 (CIT) promotes the growth of human colon cancer cells. CIT is overexpressed in human colon cancer tissues and cell lines. High expression of CIT predicts poor survival for patients with colon cancer. In colon cancer cells, CIT knockdown represses cellular proliferation and colony formation. Our in vivo xenograft experiments showed that CIT knockdown reduces the growth rate of colon cancer cells and the final tumor weight. We found that CIT knockdown induces cell cycle arrest and apoptosis in colon cancer cells. Further microarray and bioinformatics analyses indicated that CIT regulates the p53 signaling pathway, which may account for the effects of CIT on colon cancer cells. Taken together, our findings provide evidence that CIT may promote the development of colon cancer, at least in part, through the p53 signaling pathway. Therefore, CIT may be a potential therapeutic target for colon cancer treatment.


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