Inhibition by retinoids of anthralin-induced mouse epidermal ornithine decarboxylase activity and anthralin-promoted skin tumor formation.
The retinoids all-trans-retinoic acid, 13-cis-retinoic acid, 4-[2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1E- propen-1-yl]benzoic acid, 6-[1-(4-carboxyphenyl)-1E-propen-2-yl]-3,4-dihydro-4,4-dimethyl-2H -1-benzothiopyran, and 6-(5,6,7,8,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)- 2-naphthalenecarboxylic acid inhibited the induction of ornithine decarboxylase in CD-1 mouse epidermis treated with the weak tumor promoter anthralin (444 nmol). Enzyme activity reached maximal levels 48 h after the application of the promoter. This activity was most effectively inhibited when retinoids were applied to the epidermis 24 h after the promoter. These retinoids also inhibited the appearance of papillomas in mouse epidermis in the two-stage tumorigenesis model using 7,12-dimethylbenz(a)anthracene (200 nmol) as the initiator and anthralin (444 nmol) as the promoter during the 32-week period of promotion. Comparison of the doses of retinoids required to inhibit anthralin-induced ornithine decarboxylase by 50% and those required to inhibit anthralin-induced tumor promotion by 50% demonstrated that these values correlated.[1]References
- Inhibition by retinoids of anthralin-induced mouse epidermal ornithine decarboxylase activity and anthralin-promoted skin tumor formation. Dawson, M.I., Chao, W.R., Helmes, C.T. Cancer Res. (1987) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
