Caffeine suppressed gene provides further development in skin cancer prevention - Kenneth Lopez-Loo
Recent studies showed that caffeine could be added to sunscreen to provide additional protection against UV rays. Over-exposure to UV rays damages the DNA of skin cells causing an error in replication. Hence, causing skin cancer. Conney’s experiment focused on the gene Ataxia telaniectasia and Rad3 related (ATR) and its suppression under the presence of caffeine and this phenomenon effects UV damaged cells and skin cancer (Conney et al., 2011).
According to GeneCards (2011), the ATR gene codes for a protein kinase that serves as a checkpoint that prevented cells with damaged DNA to undergo the cell cycle. As a kinase, it sits along the outer membrane of cells, awaiting the targeted molecule to bind to its receptor in order for it to activate. (Campbell, 2012, p.216) The ATR kinase activates when it experience DNA stresses like UV rays and caffeine and when active, it facilitates DNA damage repair (Conney et al., 2011).
Typically, damaged cells undergo apoptosis, where the cell breaks up all its organelles and genetic material into small vesicles, disabling itself. This process of cellular suicide prevents the damaged cell from affecting its neighboring cells or replicating its error (Campbell, 2012, p.227). Therefore apoptosis is a highly effective method of eliminating potential cancerous cells before it has a chance to replicate.
When a cell gets DNA damage from UV rays, the damaged cell would seize all other functions and start repairing its genetic material; this process would be activated by ATR. If ATR were to be suppressed or inhibited, the cell would undergo apoptosis instead of going into repair, this wipes out the defective cell along with its defective genetic material (Kremer et al., 2007). Hence, lowering the chances of getting skin cancer. The notion of whether suppressed ATR played a significant role in UV damage tumorigenesis was tested by Conney’s experiement.
Conney’s study tested 2 groups of mice; one as a control and the other, an ATR deficient genetically modified mice. The GM mice with the suppressed levels of ATR were meant to act as a model for the intake of caffeine (to suppress the ATR activity) as compared to the control, which had zero alterations to the ATR gene. Both groups were chronically exposed to UV rays and the results revealed that after 19 weeks of exposure, the GM mice have 69% fewer tumors as compared to the control. In addition, the GM mice started developing tumors 3 weeks later than the control. This result highly supported Conney’s hypothesis of “the inhibition of ATR function would lead to the suppression of UV-induced tumorigenesis” (Conney et al., 2011).
As ATR gets suppressed in the presence of caffeine, cells with UV damaged DNA would go through apoptosis instead of DNA repair. This way, the DNA damaged cells that might have failed at DNA repair would be destroyed, ultimately lowering the susceptibility to obtaining skin cancer (Conney et al., 2011).. Therefore the addition of caffeine into sunscreen could enable the topical application of caffeine that would suppress ATR in skins cells. Further development would be required with regards to the whether the consumption of caffeine would have the same results as direct application (Conney et al., 2011).
· Campbell, N. et al. (2012) Campbell Biology. 9th ed. Australia: Pearson, p.214-216, 227.
· Conney, A. et al. (2011) Protection from UV-induced skin carcinogenesis by genetic inhibition of the ataxia telangiectasia and Rad3-related (ATR) kinase. PNAS, 108 (33), p.1-5.
· GeneCards (2011) ataxia telangiectasia and Rad3 related. [online] Available at: http://www.genecards.org/cgi-bin/carddisp.pl?gene=ATR [Accessed: 16 March 2012].
· Kremer, B. et al. (2007) Septins Regulate Actin Organization and Cell-Cycle Arrest through Nuclear Accumulation of NCK Mediated by SOCS7. CELL, 130 (5), p.1.