Matsushima Y, Fukasawa H, Endo Y, Hashimoto Y, Shudo K
Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Biol Pharm Bull. 1994 Sep;17(9):1292-5. doi: 10.1248/bpb.17.1292.
Human papillomavirus type 18 (HPV18) is involved in the genesis of cervical cancer through expression of its viral oncoprotein in infected cells. A tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), was found to increase the level of HPV18 transcripts in an HPV18-harboring cervical cancer cell line, HeLa. A similar increase in HPV18 expression was also observed on treatment of the cells with an oxygenated cholesterol, 3 beta,5 alpha-dihydroxycholestan-6-one (yakkasterone). The effects on HPV18 expression elicited by TPA and yakkasterone were repressed by a protein kinase inhibitor, staurosporine. Treatment of the cells with cholesterol under serum-free conditions also resulted in an apparent increase of HPV18 expression.
18型人乳头瘤病毒（HPV18）通过在受感染细胞中表达其病毒癌蛋白参与宫颈癌的发生。一种肿瘤启动子，12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA），被发现可增加携带HPV18的宫颈癌细胞系HeLa中HPV18转录本的水平。在用一种氧化胆固醇3β,5α - 二羟基胆甾烷 - 6 - 酮（牦牛甾酮）处理细胞时，也观察到HPV18表达有类似增加。TPA和牦牛甾酮对HPV18表达的影响被一种蛋白激酶抑制剂，星形孢菌素所抑制。在无血清条件下用胆固醇处理细胞也导致HPV18表达明显增加。
