Merryman J I, DeWille J W, Werkmeister J R, Capen C C, Rosol T J
Department of Veterinary Pathobiology, Ohio State University, Columbus 43210.
Endocrinology. 1994 Jun;134(6):2424-30. doi: 10.1210/endo.134.6.8194469.
The effects of human recombinant transforming growth factor (TGF)-beta 1 were determined on PTH-related protein (PTHrP) production and messenger RNA (mRNA) expression by a canine squamous carcinoma cell line (SCC 2/88) in vitro. TGF-beta increased PTHrP production in a dose- and time-dependent manner (P < 0.05) as measured by RIA, and the effects of TGF-beta treatment persisted up to 72 h after removal. TGF-beta increased PTHrP production by SCC 2/88 cells until cellular confluence, at which time there was no longer a significant increase compared to control. Actinomycin D inhibited the TGF-beta-mediated increase in PTHrP production, suggesting that TGF-beta acted in part by increasing gene transcription. SCC 2/88 cells also produced active TGF-beta as measured by a [3H]thymidine incorporation assay in mink lung epithelial cells. Exposure of SCC 2/88 cells to a neutralizing anti-TGF-beta monoclonal antibody decreased (up to 50%, P < 0.01) basal PTHrP production. TGF-beta increased PTHrP mRNA expression in a dose- and time-dependent manner as evaluated by northern blot analysis. Postconfluent SCC 2/88 cells expressed little mRNA for PTHrP, and there was only a minimal increase in PTHrP mRNA expression in postconfluent TGF-beta-treated cells. These results indicate that TGF-beta increased PTHrP production and mRNA expression in malignant keratinocytes and suggest that TGF-beta may be an important factor in the pathogenesis of humoral hypercalcemia of malignancy.
在体外,研究了人重组转化生长因子(TGF)-β1 对犬鳞状癌细胞系(SCC 2/88)甲状旁腺激素相关蛋白(PTHrP)产生及信使核糖核酸(mRNA)表达的影响。通过放射免疫分析法(RIA)测定,TGF-β 以剂量和时间依赖性方式增加 PTHrP 的产生(P < 0.05),并且在去除 TGF-β 后,其作用可持续长达 72 小时。TGF-β 使 SCC 2/88 细胞的 PTHrP 产生增加,直至细胞汇合,此时与对照组相比不再有显著增加。放线菌素 D 抑制了 TGF-β 介导的 PTHrP 产生增加,表明 TGF-β 部分通过增加基因转录发挥作用。通过貂肺上皮细胞的 [3H]胸苷掺入试验测定,SCC 2/88 细胞也产生活性 TGF-β。将 SCC 2/88 细胞暴露于中和性抗 TGF-β 单克隆抗体可降低(高达 50%,P < 0.01)基础 PTHrP 的产生。通过 Northern 印迹分析评估,TGF-β 以剂量和时间依赖性方式增加 PTHrP mRNA 的表达。汇合后的 SCC 2/88 细胞几乎不表达 PTHrP 的 mRNA,并且在汇合后经 TGF-β 处理的细胞中,PTHrP mRNA 表达仅略有增加。这些结果表明,TGF-β 增加了恶性角质形成细胞中 PTHrP 的产生和 mRNA 表达,并提示 TGF-β 可能是恶性肿瘤体液性高钙血症发病机制中的一个重要因素。