There’s been increased talk of late regarding the potential for compounds contained in coffee potentially protecting against skin cancer.

The other study that came to mind (I can’t find the article, sorry!) was one that found that coffee combined with exercise somehow mitigated the damage caused by sunburn by enhancing apoptosis of damaged cells.

This latest study looks at caffeic acid, a component of coffee, and its ability to inhibit COX-2 release following UV-B exposure:

Caffeic Acid, a Phenolic Phytochemical in Coffee, directly inhibits Fyn Kinase Activity and UVB-induced COX-2 Expression.

Carcinogenesis. 2008 Dec 10; PMID: 19073879

Kang NJ, Lee KW, Shin BJ, Jung SK, Hwang MK, Bode AM, Heo YS, Lee HJ, Dong Z.

Hormel Institute, University of Minnesota, 801 16 Avenue NE, Austin MN, USA.

Caffeic acid (3,4-dihydroxycinnamic acid) is a well-known phenolic phytochemical present in many foods, including coffee. Recent studies suggested that caffeic acid exerts anticarcinogenic effects, but little is known about the underlying molecular mechanisms and specific target proteins. In this study, we found that Fyn, one of the members of the nonreceptor protein tyrosine kinase family, was required for UVB-induced COX-2 expression, and caffeic acid suppressed UVB-induced skin carcinogenesis by directly inhibiting Fyn kinase activity. Caffeic acid more effectively suppressed UVB-induced COX-2 expression and subsequent prostaglandin E(2) (PGE(2)) production in JB6 P+ mouse skin epidermal (JB6 P+) cells compared to chlorogenic acid (5-O-cafeoylquinic acid), an ester of caffeic acid with quinic acid. Data also revealed that caffeic acid more effectively induced the down-regulation of COX-2 expression at the transcriptional level mediated through the inhibition of activator protein (AP)-1 and nuclear factor (NF)-kappaB transcription activity compared to chlorogenic acid. Fyn kinase activity was suppressed more effectively by caffeic acid than by chlorogenic acid, and downstream mitogen-activated protein (MAP) kinases were subsequently blocked. Pharmacological Fyn kinase inhibitor (PP2 and leflunomide) data also revealed that Fyn is involved in UVB-induced COX-2 expression mediated through the phosphorylation of MAP kinases in JB6 P+ cells. Pull-down assays revealed that caffeic acid directly bound with Fyn and noncompetitively with ATP. In vivo data from mouse skin also supported the idea that caffeic acid suppressed UVB-induced COX-2 expression by blocking Fyn kinase activity. These results suggested that this compound could act as a potent chemopreventive against skin cancer.