Hoshino H, Miwa M, Fujiki H
Int J Cancer. 1983 Apr 15;31(4):509-13. doi: 10.1002/ijc.2910310418.
The effects of tumor promoters on the expression of murine leukemia virus (MuLV) were studied in tissue culture. Dihydroteleocidin B, an indole alkaloid, recently found to be a tumor promoter, enhanced not only the production of Moloney MuLV (M-MuLV) by a mouse fibroblast cell line, C3H2K, persistently infected with M-MuLV, but also growth on the C3H2K cells. The production of infectious M-MuLV by M-MuLV-infected C3H2K cells that had been treated with dihydroteleocidin B for 1-7 days was four or five times higher than that of control cells. C3H2K cells grew faster and became stationary at higher cell densities in the presence of dihydroteleocidin B than in its absence. The tumor-promoting phorbol ester phorbol-12, 13-didecanoate and 12-O-tetradecanoylphorbol-13-acetate also enhanced the production of M-MuLV, but their effects were not so strong as that of dihydroteleocidin B. These tumor promoters, however, did not induce production of endogenous MuLV in C3H2K or K-BALB cells.
在组织培养中研究了肿瘤启动子对鼠白血病病毒(MuLV)表达的影响。二氢替告吉宁B,一种吲哚生物碱,最近被发现是一种肿瘤启动子,它不仅增强了持续感染莫洛尼MuLV(M-MuLV)的小鼠成纤维细胞系C3H2K产生M-MuLV的能力,还增强了其在C3H2K细胞上的生长。用二氢替告吉宁B处理1-7天的M-MuLV感染的C3H2K细胞产生的传染性M-MuLV比对照细胞高四到五倍。在存在二氢替告吉宁B的情况下,C3H2K细胞生长更快,并且在比不存在时更高的细胞密度下达到静止状态。促肿瘤的佛波酯佛波醇-12,13-二癸酸酯和12-O-十四酰佛波醇-13-乙酸酯也增强了M-MuLV的产生,但其效果不如二氢替告吉宁B强。然而,这些肿瘤启动子并未诱导C3H2K或K-BALB细胞产生内源性MuLV。