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Environ Toxicol. 2017 Feb;32(2):690-704. doi: 10.1002/tox.22271. Epub 2016 Apr 18.

Cigarette smoke extracts induced the colon cancer migration via regulating epithelial mesenchymal transition and metastatic genes in human colon cancer cells.

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Laboratory of Biochemistry and Immunology, Department of Veterinary Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.
Inhalation Toxicology Center, Jeonbuk Department of Non-Human Primate, Korea Institute of Toxicology, Jeonbuk, Republic of Korea.
Biosafety Research Institute and Laboratory of Pathology (BK21 Plus Program), Department of Veterinary Medicine, College of Veterinary Medicine, Chonbuk National University, Iksan, Republic of Korea.
Department of Pharmaceutical Sciences, College of Pharmacy, Dongguk University, Goyang, Gyeonggi-Do, Republic of Korea.


There was considerable evidence that exposure to cigarette smoke is associated with an increased risk for colon cancer. Nevertheless, the mechanism underlying the relationship between cigarette smoking and colon cancer remains unclear. Moreover, there were only a few studies on effects of complexing substance contained in cigarette smoke on colon cancer. Thus, we further investigated whether cigarette smoke extract (CSE) affects the cell cycle, apoptosis and migration of human metastatic colon cancer cells, SW-620. MTT assay revealed that SW-620 cell proliferation was significantly inhibited following treatments with all CSEs, 3R4F, and two-domestic cigarettes, for 9 days in a concentration-dependent manner. Moreover, CSE treatments decreased cyclin D1 and E1, and increased p21 and p27 proteins by Western blot analysis in SW-620 cells. Additionally, the treatment of the cells with CSE contributed to these effects expressing by apoptosis-related proteins. An increased migration or invasion ability of SW-620 cells following CSE treatment was also confirmed by a scratch or fibronectin invasion assay in vitro. In addition, the protein levels of E-cadherin as an epithelial maker were down-regulated, while the mesenchymal markers, N-cadherin, snail, and slug, were up-regulated in a time-dependent manner. A metastatic marker, cathepsin D, was also down-regulated by CSE treatment. Taken together, these results indicate that CSE exposure in colon cancer cells may deregulate the cell growth by altering the expression of cell cycle-related proteins and pro-apoptotic protein, and stimulate cell metastatic ability by altering epithelial-mesenchymal transition (EMT) markers and cathepsin D expression.


apoptosis; cell cycle; cigarette smoke extract; colon cancer cells; metastasis

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