Effect of truncated neurokinin‐1 receptor expression changes on the interaction between human breast cancer and bone marrow‐derived mesenchymal stem cells
Effect of truncated neurokinin‐1 receptor expression changes on the interaction between human breast cancer and bone marrow‐derived mesenchymal stem cells
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DOI：
10.1111/gtc.12168
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发表时间：
2014-09
期刊：
影响因子：
2.1
通讯作者：
Yunli Zhou;Duo Zuo;Meng Wang;Yongci Zhang;Man Yu;Jie Yang;Z. Yao
中科院分区：
文献类型：
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作者：
Yunli Zhou;Duo Zuo;Meng Wang;Yongci Zhang;Man Yu;Jie Yang;Z. Yao
先前对乳腺癌细胞系的研究表明，截断的神经激肽受体- 1 （NK1R‐Tr）能够促进乳腺细胞的恶性转化，并且NK1R‐Tr可能有助于肿瘤进展并促进人类乳腺癌的远处转移。乳腺癌和骨髓来源的人间充质干细胞（HMSC - bm）共培养模型显示，HMSC - bm抑制乳腺癌细胞的生长，并在早期阶段进入骨髓。NK1R‐Tr的下调可能是维持骨髓基质中乳腺癌细胞静止表型的关键因素。基质衍生因子（SDF）‐1α在乳腺癌细胞中的表达与NK1R‐Tr的表达呈负相关。HMSC - bm分泌SDF - 1α可能通过下调NK1R - Tr的表达来维持骨髓基质中乳腺癌细胞的静止表型。在乳腺癌细胞中，转化生长因子（TGF）‐β1的表达与NK1R‐Tr的表达呈正相关。在共培养系统中，MDA - MB - 231 - TGF - β 1i （TGF - β基因被特异性shRNA抑制）细胞能够快速附着在HMSC - bm上，这表明TGF - β1也是维持骨髓基质中乳腺癌细胞静止表型的关键因素。然而，详细的机制仍然不清楚，可能涉及其他分子，除了NK1R‐Tr。
Previous studies in breast cancer cell lines showed that truncated neurokinin receptor‐1 (NK1R‐Tr) was able to promote malignant transformation of breast cells, and NK1R‐Tr may contribute to tumor progression and promote distant metastasis in human breast cancer. A co‐culture model of breast cancer and bone marrow‐derived human mesenchymal stem (HMSC‐bm) cells showed that HMSC‐bm inhibited the growth of breast cancer cells and entered the bone marrow at early stages. Down‐regulation of NK1R‐Tr may be a key factor in maintaining the quiescent phenotype of breast cancer cells among bone marrow stroma. Stromal‐derived factor (SDF)‐1α expression was negatively correlated with NK1R‐Tr expression in breast cancer cells. Secretion of SDF‐1α by HMSC‐bm may maintain the quiescent phenotype of breast cancer cells among bone marrow stroma by down‐regulating NK1R‐Tr expression. Transforming growth factor (TGF)‐β1 expression was positively associated with NK1R‐Tr expression in breast cancer cells. In a co‐culture system, MDA‐MB‐231‐TGF‐β1I (TGF‐β genes were suppressed using specific shRNA) cells were able to attach to HMSC‐bm quickly, indicating that TGF‐β1 was also a key factor for maintaining the quiescent phenotype of breast cancer cells in bone marrow stroma. However, the detailed mechanism still remained unclear and could involve other molecules, in addition to NK1R‐Tr.