一項(xiàng)8月15日發(fā)表的美國研究表明,，咖啡通過殺死可能轉(zhuǎn)化為腫瘤的受損細(xì)胞，有助降低罹患皮膚癌風(fēng)險,。
這項(xiàng)研究顯示,，適量飲用咖啡甚至只將咖啡應(yīng)用于皮膚，可能對避免患上非黑素瘤有助,。
研究人員利用一種受到遺傳性轉(zhuǎn)變,、抑制ATP蛋白的老鼠做實(shí)驗(yàn)，他們發(fā)現(xiàn),，這種老鼠即使曝露于紫外線,，也能抵御患癌癥。
先前研究提出,，每天飲用一杯含咖啡因咖啡,，可以啟動抑制ATP蛋白的效果,，繼而觸發(fā)受紫外線照射而受損的細(xì)胞死亡。
接受實(shí)驗(yàn)的老鼠最終都患上癌癥,，但比普通老鼠晚3個星期,。經(jīng)過19個星期照射紫外線后，受轉(zhuǎn)變老鼠產(chǎn)生腫瘤比例比對比組低69%,，患侵入性腫瘤比例低4倍,。
不過，這種抵御性效果有限,。經(jīng)過34個星期照射紫外線,，所有老鼠都產(chǎn)生腫瘤。研究報告作者之一阿倫·科菲告訴法新社記者：“最終,，如果你處理（照射）他們足夠時間,，老鼠都會患癌癥，所以這不是100%的防御,。實(shí)際上,，使用任何致癌物質(zhì)處理，所有動物最終都會患癌癥,。”
科菲和他的研究小組已經(jīng)證實(shí)最初的假設(shè),，飲用或在皮膚上應(yīng)用咖啡，可以起到抑制ATP蛋白作用,。他們說,，需要更多研究，看看是否對人類有效,。
皮膚癌是美國最常見的一種癌癥,，根據(jù)美國國家癌癥研究所數(shù)據(jù)，美國每年新增100萬個皮膚癌病例,。非黑素瘤是最常診斷出的皮膚癌,，如果發(fā)現(xiàn)及時，通?？梢灾斡?。(生物谷 Bioon.com)
doi:10.1073/pnas.1111378108
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PMID:
Protection from UV-induced skin carcinogenesis by genetic inhibition of the ataxia telangiectasia and Rad3-related (ATR) kinase
Kawasumi, Masaoki; Lemos, Bianca; Bradner, James E.; Thibodeau, Renee; Kim, Yong-son; Schmidt, Miranda; Higgins, Erin; Koo, Sang-wahn; Angle-Zahn, Aimee; Chen, Adam; Levine, Douglas; Nguyen, Lynh; Heffernan, Timothy P.; Longo, Isabel; Mandinova, Anna; Lu, Yao-Ping; Conney, Allan H.; Nghiem, Paul
Multiple human epidemiologic studies link caffeinated (but not decaffeinated) beverage intake with significant decreases inseveral types of cancer, including highly prevalent UV-associated skin carcinomas. The mechanism by which caffeine protectsagainst skin cancer is unknown. Ataxia telangiectasia and Rad3-related (ATR) is a replication checkpoint kinase activatedby DNA stresses and is one of several targets of caffeine. Suppression of ATR, or its downstream target checkpoint kinase1 (Chk1), selectively sensitizes DNA-damaged and malignant cells to apoptosis. Agents that target this pathway are currentlyin clinical trials. Conversely, inhibition of other DNA damage response pathways, such as ataxia telangiectasia mutated (ATM)and BRCA1, promotes cancer. To determine the effect of replication checkpoint inhibition on carcinogenesis, we generated transgenicmice with diminished ATR function in skin and crossed them into a UV-sensitive background, Xpc?/?. Unlike caffeine, this genetic approach was selective and had no effect on ATM activation. These transgenic mice were viableand showed no histological abnormalities in skin. Primary keratinocytes from these mice had diminished UV-induced Chk1 phosphorylationand twofold augmentation of apoptosis after UV exposure (P = 0.006). With chronic UV treatment, transgenic mice remained tumor-free for significantly longer (P = 0.003) and had 69% fewer tumors at the end of observation of the full cohort (P = 0.019), compared with littermate controls with the same genetic background. This study suggests that inhibition of replicationcheckpoint function can suppress skin carcinogenesis and supports ATR inhibition as the relevant mechanism for the protectiveeffect of caffeinated beverage intake in human epidemiologic studies.
