Zhao X, van Steenbrugge G J, Schröder F H
Department of Urology, Erasmus University, Rotterdam, The Netherlands.
Urol Res. 1992;20(3):193-7. doi: 10.1007/BF00299716.
Two sublines, the hormone-sensitive LNCaP-FGC and the insensitive LNCaP-r (resistant) carcinoma cell lines, originating from the parental human prostatic carcinoma cell line LNCaP were tested for sensitivity to human tumor necrosis factor-alpha (TNF) using the MTT assay. Irrespective of the culture conditions, i.e., whether FGC cell growth was hormone stimulated or hormone deprived, a clear dose-related response was observed between the concentration of TNF (range: 5-5000 U/ml) in the culture medium and the percentage of growth inhibition. In medium containing androgen-depleted serum, in which FGC cells showed reduced proliferative activity, the percentage of inhibition by a concentration of 100 U/ml TNF was substantially higher than that found in hormone-stimulated cells (90% and 60%, respectively). In contrast to the FGC cells, the hormone-insensitive LNCaP-r cells were almost completely resistant to the action of TNF. Growth of the FGC cells was almost completely inhibited, whereas growth of the LNCaP-r cells was retarded with only 20% at dosages up to 5000 U/ml. This substantial difference in TNF responsiveness could not be ascribed to differences in TNF-binding capacity, as both the FGC and LNCaP-r cells were found to contain identical numbers of TNF-receptors (approximately 1000 sites/cell). A possible association between hormone responsiveness and TNF sensitivity is suggested for these LNCaP sublines.
使用MTT分析法对源自亲代人前列腺癌细胞系LNCaP的两个亚系,即激素敏感的LNCaP-FGC和不敏感的LNCaP-r(抗性)癌细胞系进行了人肿瘤坏死因子-α(TNF)敏感性测试。无论培养条件如何,即无论FGC细胞生长是受激素刺激还是激素剥夺,在培养基中TNF浓度(范围:5 - 5000 U/ml)与生长抑制百分比之间均观察到明显的剂量相关反应。在含有雄激素耗尽血清的培养基中,FGC细胞的增殖活性降低,100 U/ml TNF浓度的抑制百分比显著高于激素刺激细胞中的抑制百分比(分别为90%和60%)。与FGC细胞相反,激素不敏感的LNCaP-r细胞几乎对TNF的作用完全抗性。FGC细胞的生长几乎完全被抑制,而LNCaP-r细胞的生长在高达5000 U/ml的剂量下仅被抑制20%。TNF反应性的这种显著差异不能归因于TNF结合能力的差异,因为发现FGC和LNCaP-r细胞所含的TNF受体数量相同(约1000个位点/细胞)。对于这些LNCaP亚系,提示了激素反应性与TNF敏感性之间可能存在关联。