Research Papers:
Loss of endothelial cell-specific molecule 1 promotes the tumorigenicity and metastasis of prostate cancer cells through regulation of the TIMP-1/MMP-9 expression
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Abstract
Chien-Min Chen1,2, Chu-Liang Lin3, Hui-Ling Chiou4, Shu-Ching Hsieh4, Chia-Liang Lin3, Chun-Wen Cheng3, Chia-Hung Hung3, Jen-Pi Tsai5,6, Yi-Hsien Hsieh3,7,8
1Division of Neurosurgery, Department of Surgery, Changhua Christian Hospital, Changhua, Taiwan
2School of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
3Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan
4School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan
5School of Medicine, Tzu Chi University, Hualien, Taiwan
6Division of Nephrology, Department of Internal Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan
7Department of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung, Taiwan
8Clinical laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan
Correspondence to:
Jen-Pi Tsai, email: [email protected]
Yi-Hsien Hsieh, email: [email protected]
Keywords: prostate cancer cells, endothelial cell specific molecule 1, tumorigenicity, metastasis, epithelial-mesenchymal transition
Received: August 10, 2016 Accepted: January 04, 2017 Published: January 17, 2017
ABSTRACT
The Endothelial cell specific molecule-1 (ESM1) protein has been involved in proliferation and metastatic progression in multiple tumors. However, there are no studies regarding the mechanism of ESM1 in prostate cancer. We found that ESM1 knockdown in prostate cancer cells resulted in increased cell proliferation and colony formation ability response evidenced by decreased expression of p21 and increased expression of cyclin D1 in prostate cancer cells. Moreover, we revealed that knockdown ESM1 also induced the epithelial-mesenchymal transition (EMT), motility and invasiveness in accordance with the upregulated the MMP-9 expression, while downregulated the TIMP-1 expression. Recombinant human (Rh) TIMP-1 significantly attenuated ESM1-mediated cell migration and invasion. Additionally, ESM1 knockdown increased in vivo tumorigenicity and metastasis of prostate cancer cells. These findings provide the first evidence that the imbalance of MMP-9/TIMP-1, is one of the regulation mechanisms by which ESM1 promotes tumorigenicity and metastasis of prostate cancer cells.
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PII: 14684