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The synthetic retinoid adapalene inhibits proliferation and induces apoptosis in colorectal cancer cells in vitro

✍ Scribed by Matthias Ocker; Christoph Herold; Marion Ganslmayer; Eckhart G. Hahn; Detlef Schuppan

Publisher
John Wiley and Sons
Year
2003
Tongue
French
Weight
295 KB
Volume
107
Category
Article
ISSN
0020-7136

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✦ Synopsis

Abstract

Chemotherapy of advanced stages of colorectal carcinoma is unsatisfactory. Retinoids inhibit cell growth and induce apoptosis in a variety of human malignancies. We compared the effect of the synthetic retinoid adapalene (ADA) and 9‐cis‐retinoic acid (CRA) on carcinoma cell lines in vitro. Colon carcinoma cell lines CC‐531, HT‐29 and LOVO as well as human foreskin fibroblasts were exposed to different concentrations of ADA and CRA for 3–72 hr. Proliferation was assessed by BrdU incorporation and apoptosis by FACS analysis. Breakdown of ΔΨ~m~ was determined by JC‐1 staining and activity of caspases 3 and 8, by a colorimetric assay. Quantitative Western blots were performed to detect changes in bax, bcl‐2 and caspase‐3. Both retinoic derivatives suppressed DNA synthesis and induced apoptosis in all tested cell lines time‐ and dose‐dependently. While the natural retinoid CRA showed moderate antiproliferative and proapoptotic effects only at the highest concentration (10^–4^ M), the synthetic retinoic ADA was significantly more effective, showing remarkable effects even at 10^–5^ M. ADA and CRA disrupt ΔΨ~m~ and induce caspase‐3 activity in responsive tumor cells. Quantitative Western blots showed a shift of the bax:bcl‐2 ratio toward proapoptotic bax in ADA‐treated cells. Our results clearly indicate the superiority of ADA compared to CRA. Therefore, we suggest that ADA may be far more suitable as an adjunctive therapeutic agent for treatment of colon cancer in vivo. © 2003 Wiley‐Liss, Inc.

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The above article, published online on April 10 2008 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor in Chief and Wiley Periodicals, Ltd. The retraction has been agreed due to data duplication, both from previous papers from the same group