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Molecular Oncology Unit, Cancer Research Center of Hawaii, University of Hawaii, Honolulu, Hawaii 96813
Epidemiological evidence and studies in whole animals and cell culture have indicated that carotenoids have cancer chemopreventive action. In mouse C3H10T1/2 cells, this activity is highly correlated with the ability of carotenoids to up-regulate gap junctional intercellular communication. Here, we report that in mouse cells, carotenoids increase the expression of connexin43, a gene that encodes a major gap junction protein. This effect appears unrelated to their provitamin A or antioxidant properties, since carotenoids with and without provitamin A activity increased levels of connexin43 mRNA and protein, whereas the antioxidants methyl-bixin and 
-tocopherol were inactive. Moreover, the active carotenoid canthaxanthin did not induce the vitamin A-inducible gene retinoic acid receptor-ß. Connexin43 is the first carotenoid-inducible gene described in mammals. By indicating an additional pathway through which carotenoids function, these data provide a mechanistic basis for cancer chemoprevention by carotenoids and may lead to a re-evaluation of carotenoid physiology.
1 This research was supported by Grant BC686 from the American Cancer Society.
2 To whom requests for reprints should be addressed, at University of Hawaii at Manoa, Cancer Research Center, Department of Molecular Oncology, 1236 Lauhala Street, Honolulu, HI 96813.
Received 4/23/92. Accepted 8/ 3/92.
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