Inhibition of UVB-induced nonmelanoma skin cancer: a path from tea to caffeine to exercise to decreased tissue fat.

Abstract

Oral administration of green tea, black tea, or caffeine (but not the decaffeinated teas) inhibited ultraviolet B radiation (UVB)-induced skin carcinogenesis in SKH-1 mice. Studies with caffeine indicated that its inhibitory effect on the ATR/Chk1 pathway is an important mechanism for caffeine's inhibition of UVB-induced carcinogenesis. The regular teas or caffeine increased locomotor activity and decreased tissue fat. In these studies, decreased dermal fat thickness was associated with a decrease in the number of tumors per mouse. Administration of caffeine, voluntary exercise, and removal of the parametrial fat pads all stimulated UVB-induced apoptosis, inhibited UVB-induced carcinogenesis, and stimulated apoptosis in UVB-induced tumors. These results suggest that caffeine administration, voluntary exercise, and removal of the parametrial fat pads inhibit UVB-induced carcinogenesis by stimulating UVB-induced apoptosis and by enhancing apoptosis in DNA-damaged precancer cells and in cancer cells. We hypothesize that tissue fat secretes antiapoptotic adipokines that have a tumor promoting effect.

• Authors: Allan H Conney, You-Rong Lou, Paul Nghiem, Jamie J Bernard, George C Wagner, Yao-Ping Lu
• Journal: Topics in current chemistry (Top Curr Chem) Vol. 329 Pg. 61-72 ( 2013) ISSN: 0340-1022 [Print] Germany
• PMID: 22752580 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)

Chemical References

• Tea
• Caffeine

Topics

• Adipose Tissue (drug effects)
• Administration, Oral
• Animals
• Apoptosis (radiation effects)
• Caffeine (administration & dosage, pharmacology)
• Mice
• Neoplasms, Radiation-Induced (pathology, prevention & control)
• Physical Conditioning, Animal
• Skin Neoplasms (etiology, pathology, prevention & control)
• Tea
• Ultraviolet Rays