Suppr超能文献

转化生长因子-β对体外培养的鳞状癌细胞系甲状旁腺激素相关蛋白生成及核糖核酸表达的影响

Effects of transforming growth factor-beta on parathyroid hormone-related protein production and ribonucleic acid expression by a squamous carcinoma cell line in vitro.

作者信息

Merryman J I, DeWille J W, Werkmeister J R, Capen C C, Rosol T J

机构信息

Department of Veterinary Pathobiology, Ohio State University, Columbus 43210.

出版信息

Endocrinology. 1994 Jun;134(6):2424-30. doi: 10.1210/endo.134.6.8194469.

Abstract

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.

摘要

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。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验