Journal Article

Cigarette smoke exposure increases ulcerative colitis-associated colonic adenoma formation in mice

Edgar S.L. Liu, Yi-Ni Ye, Vivian Y. Shin, Siu-Tsan Yuen, Suet-Yi Leung, Benjamin C.Y. Wong and Chi-Hin Cho

in Carcinogenesis

Volume 24, issue 8, pages 1407-1413
Published in print August 2003 | ISSN: 0143-3334
Published online August 2003 | e-ISSN: 1460-2180 | DOI:
Cigarette smoke exposure increases ulcerative colitis-associated colonic adenoma formation in mice

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Both chronic ulcerative colitis and smoking are associated with colorectal cancer in humans. In the present study, we investigated the effects of cigarette smoke (CS) exposure on inflammation-associated tumorigenesis in the mouse colon. Male balb/c mice were allocated into six groups: control, CS (2%), CS (4%), colitis, colitis + CS (2%) and colitis + CS (4%). They were given water or 3% dextran sulfate sodium (DSS) in drinking water for 7 days to induce colitis, with or without 1 h daily exposure to 2 or 4% CS. They were then allowed to drink water for 14 days. The cycle of 7 day DSS ± CS/14 day H2O treatments were repeated twice. Mice were killed immediately or 1 month after the three cycles of treatments. Results indicated colonic adenoma was only found in the colitis group (one out of 11), Colitis + CS (2%) group (seven out of 12) and colitis + CS (4%) group (four out of five) 1 month after three cycles of DSS and/or CS treatment. CS exposure dose-dependently increased adenoma formation in mice with inflamed mucosa. CS exposure plus colitis was strongly associated with a high incidence of dysplasia (P < 0.01) and adenocarcinoma formation (P < 0.01) compared with induction of colitis alone. Colitis induced cell proliferation and apoptosis in colonic tissues. Cigarette smoking significantly attenuated the apoptotic effect by DSS probably via the induction of anti-apoptotic protein bcl-2. The ratio of apoptosis over proliferation was also significantly lower in the colitis + CS groups. Vascular endothelial growth factor and angiogenesis in the colon were also increased by cigarette smoking in animals with colitis. In conclusion, CS promotes inflammation-associated adenoma/adenocarcinoma formation in the mouse colon in a dose-dependent manner. This tumor development is associated with the inhibition of cellular apoptosis and supported by increased angiogenesis.

Keywords: CS, cigarette smoke; DSS, dextran sulfate sodium; PCNA, proliferating cell nuclear antigen; VEGF, vascular endothelial growth factor

Journal Article.  4638 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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