BMP9 regulates cross-talk between breast cancer cells and bone marrow-derived mesenchymal stem cells

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• 作者：Shaoheng Wan (1)
  Yuehong Liu (1)
  Yaguang Weng (1)
  Wei Wang (1)
  Wei Ren (2)
  Chang Fei (1)
  Yingying Chen (1)
  Zhihui Zhang (1)
  Ting Wang (1)
  Jinshu Wang (1)
  Yayun Jiang (1)
  Lan Zhou (1)
  Tongchuan He (3)
  Yan Zhang (1)
  
• 关键词：BMP9 ; Breast cancer ; Bone marrow ; derived mesenchymal stem cells ; Cross ; talk ; RANKL/RANK axis
• 刊名：Cellular Oncology
• 出版年：2014
• 出版时间：October 2014
• 年：2014
• 卷：37
• 期：5
• 页码：363-375
• 全文大小：4,321 KB
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• 作者单位：Shaoheng Wan (1)
  Yuehong Liu (1)
  Yaguang Weng (1)
  Wei Wang (1)
  Wei Ren (2)
  Chang Fei (1)
  Yingying Chen (1)
  Zhihui Zhang (1)
  Ting Wang (1)
  Jinshu Wang (1)
  Yayun Jiang (1)
  Lan Zhou (1)
  Tongchuan He (3)
  Yan Zhang (1)
  
  1. Key Laboratory of Diagnostic Medicine designated by the Ministry of Education, Chongqing Medical University, 1 Yixueyuan Road, Yuzhong District, Chongqing, 400016, China
  2. Department of General Surgery, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing, 400042, China
  3. Molecular Oncology Laboratory, Department of Surgery, The University of Chicago Medical Center, Chicago, IL, USA
  
• ISSN：2211-3436

文摘

Purpose Breast cancer cells frequently metastasize to distant organs, including bone. Interactions between breast cancer cells and the bone microenvironment are known to enhance tumor growth and osteolytic damage. Here we investigated whether BMP9 (a secretary protein) may change the bone microenvironment and, by doing so, regulate the cross-talk between breast cancer cells and bone marrow-derived mesenchymal stem cells. Methods After establishing a co-culture system composed of MDA-MB-231breast cancer cells and HS-5 bone marrow-derived mesenchymal stem cells, and exposure of this system to BMP9 conditioned media, we assessed putative changes in migration and invasion capacities of MDA-MB-231 cells and concomitant changes in osteogenic marker expressionin HS-5 cells and metastases-related genes in MDA-MB-231 cells. Results We found that BMP9 can inhibit the migration and invasion of MDA-MB-231 cells, and promote osteogenesis and proliferation of HS-5 cells, in the co-culture system. We also found that the BMP9-induced inhibition of migration and invasion of MDA-MB-231 cells may be caused by a decreased RANK ligand (RANKL) secretion by HS-5 cells, leading to a block in the AKT signaling pathway. Conclusions From our data we conclude that BMP9 inhibits the migration and invasion of breast cancer cells, and promotes the osteoblastic differentiation and proliferation of bone marrow-derived mesenchymal stem cells by regulating cross-talk between these two types of cells through the RANK/RANKL signaling axis.