Lavrovsky V, Dong Z, Ma W Y, Colburn N
Laboratory of Viral Carcinogenesis, NCI-FCRDC, Frederick, Maryland 21702-1201, USA.
In Vitro Cell Dev Biol Anim. 1996 Apr;32(4):234-7. doi: 10.1007/BF02722951.
Transformed JB6 cells can be stably reverted to nontransformed phenotype by AP-1 inhibiting gluccorticoid fluocinolone (FA) and cAMP elevator forskolin (FN), yielding stable revertants of promotion resistant (P-) and promotion sensitive (P+) phenotypes. AP-1 activity of nontransformed P- and P+ revertant clones was decreased under a variety of experimental conditions compared with their transformed counterparts. Moreover, AP-1 activity in P+ cells under anchorage-independent conditions was induced by 12-0-tetradecanoyl-phorbol-13-acetate (TPA) while AP-1 activity in the reverted P- cells was not induced, just as observed for the original P+ and P- variants. Taken together these data suggest that changes in AP-1 activity may be one key mediator not only of forward progression but also of reversion of tumor cells to nontransformed phenotype. In addition, the higher transfection efficiency of the new reverted P- and P+ cells renders them useful for studying the role of transcription factors in tumor promotion.
转化的JB6细胞可通过抑制AP-1的糖皮质激素氟轻松（FA）和cAMP增强剂福斯可林（FN）稳定地回复到未转化表型，产生促进抗性（P-）和促进敏感（P+）表型的稳定回复株。与转化的对应细胞相比，在各种实验条件下，未转化的P-和P+回复株克隆的AP-1活性降低。此外，在非贴壁条件下，P+细胞中的AP-1活性由12-0-十四烷酰佛波醇-13-乙酸酯（TPA）诱导，而回复的P-细胞中的AP-1活性未被诱导，正如原始P+和P-变体所观察到的那样。综合这些数据表明，AP-1活性的变化可能不仅是肿瘤细胞向前发展的一个关键介质，也是肿瘤细胞回复到未转化表型的关键介质。此外，新回复的P-和P+细胞的较高转染效率使其可用于研究转录因子在肿瘤促进中的作用。
