Siegfried J M, Kaufman D G
Int J Cancer. 1983 Oct 15;32(4):423-9. doi: 10.1002/ijc.2910320405.
The tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) was found to increase the incidence of phenotypic alterations induced by the direct-acting carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in human endometrial stromal cells. Following carcinogen treatment, changes in saturation density, gamma-glutamyltranspeptidase expression, morphology, and growth in selective media were enhanced in cell cultures subjected to continuous TPA exposure as compared to cultures receiving ethanol vehicle. This enhancement may have resulted, at least in part, from selection of cells altered by carcinogen, as evidenced by differences in the colony-forming abilities of MNNG-treated and control cultures after prolonged TPA exposure, and by differences in morphologic response to TPA challenge in these two populations.
肿瘤促进剂12-O-十四烷酰佛波醇-13-乙酸酯（TPA）被发现可增加直接作用致癌物N-甲基-N'-硝基-N-亚硝基胍（MNNG）诱导人子宫内膜基质细胞发生表型改变的发生率。与接受乙醇载体的培养物相比，在连续TPA暴露的细胞培养物中，致癌物处理后，饱和密度、γ-谷氨酰转肽酶表达、形态和在选择性培养基中的生长变化增强。这种增强可能至少部分是由于选择了被致癌物改变的细胞，延长TPA暴露后MNNG处理组和对照组培养物集落形成能力的差异以及这两组细胞对TPA刺激的形态学反应差异证明了这一点。
