天津医药

• 论著 •    

乳腺癌细胞通过PTHrP调节成骨细胞MCP-1基因表达

张珊珊1,李晓霞2,王宝利3   

  1. 1. 天津医科大学代谢病医院内分泌研究所
    2. 天津医科大学基础医学院微生物学教研室
    3. 天津医科大学代谢病医院内分泌研究所、卫生部激素与发育重点实验室
  • 收稿日期:2009-09-27 修回日期:2009-10-19 出版日期:2010-11-15 发布日期:2010-11-15
  • 通讯作者: 王宝利

Regulation of MCP-1 in osteoblasts by PTHrP in breast cancer cells

  • Received:2009-09-27 Revised:2009-10-19 Published:2010-11-15 Online:2010-11-15

摘要： 摘要 目的：探讨乳腺癌细胞分泌的PTHrP对成骨细胞MCP-1基因表达的调节作用。方法：观察PTHrP对成骨细胞MCP-1基因表达的调节规律；构建shRNA重组质粒PTH1R/pRNAT，将其转染至成骨细胞，建立稳定表达的细胞系PTH1R/UMR106；将乳腺癌细胞MDA-MB231 条件培养基（CM）分别作用于UMR106和PTH1R/UMR106，通过半定量RT-PCR法测定MCP-1的mRNA表达。

关键词: 乳腺癌, PTHrP, 成骨细胞, MCP-1

Abstract: Abstract Objective: To identify regulation of MCP-1 in osteoblasts by PTHrP in breast cancer cells. Method: Osteoblast-like UMR106 cells were treated with 10-8 M PTHrP (1–34) for different time intervals and expression of MCP-1 was studied by using semiquantitative RT-PCR. Recombinant shRNA plsmid PTH1R/pRNAT was constructed, transfected into UMR106 cells, and stable PTH1R/UMR106 cells were established in which PTH1R expression was knocked-down. Thereafter, the conditioned medium (CM) of breast cancer MDA-MB231 was added to UMR-106 and PTH1R/UMR106 cultures respectively. The mRNA of MCP-1 treated by PTHrP and CM of breast cancer was examined by RT-PCR. Result: PTHrP induced expression of MCP-1 in UMR106 cells and the induction began at 3 h and reached maximum at 6 h. Treatment of UMR106 cells with CM of MDA-MB231 also significantly induced mRNA of MCP-1, and this effect was blocked by the knockdown of PTH1R in UMR106 cells. Conclusion: Breast cancers upregulated MCP-1 level in osteoblasts through expression of PTHrP.

Key words: breast cancer, PTHrP, osteoblasts, MCP-1