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

Abstract

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. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 690-704, 2017.

Changes in Body Composition During Adjuvant FOLFOX Chemotherapy and Overall Survival in Non-Metastatic Colon Cancer

“…In addition, a recent meta-analysis reported random-effects HR estimates (95% CI) for all-cause mortality of 1.26 (1.15-1.37) for current smokers compared with never smokers, which indicated that smoking had detrimental effects on survival even after CRC diagnosis [36]. There is some in vitro evidence that smoking could stimulate cell metastatic ability by altering epithelial-mesenchymal transition and influence chemotherapy efficacy by inducing metabolic and epigenetic alterations [37,38]. Smoking showed a strong influence on the natural history of chronic obstructive pulmonary disease (COPD) and smoking related COPD was a significant predictor of more visit to emergency room and hospital readmission in colon cancer patients treated with adjuvant chemotherapy [39,40].…”

Calotropin regulates the apoptosis of non‑small cell cancer by regulating the cytotoxic T‑lymphocyte associated antigen 4‑mediated TGF‑β/ERK signaling pathway

“…The pro-apoptosis capacity and potential mechanism underlying Calotropin-mediated apoptosis in NSCLC cells were also analyzed. The results demonstrated that Calotropin inhibited H358 cell growth, migration and invasion by decreasing FN and VIM, and increasing Eca expression levels ( 24 , 25 ). It was also revealed that Calotropin treatment promoted apoptosis by upregulating pro-apoptosis gene and downregulating anti-apoptosis protein expression.…”

Differential Effects between Cigarette Total Particulate Matter and Cigarette Smoke Extract on Blood and Blood Vessel

“…TPM and CSE were prepared as described in our previous studies (9). University of Kentucky 3R4F reference cigarettes were smoked on a 30-port smoking machine (CH Technologies, Westwood, NJ, USA) at 35-mL puff volume, 2-sec puff duration and 60 sec between puffs, in conformity with ISO standard 3308.…”