中文摘要：

增长证据证明了方面人口(SP ) 房间为癌症干细胞(CSC ) 被充实为癌症恶意负责。在这研究， SP 技术被用来在在 vitro 为增长有优异潜力的人的胆囊癌症房间线 GBC-SD，和 SP 房间孤立 SP 房间的小 subpopulation，在 vivo 的 tumorigenesis 被识别。重要地，许多 GBC-SD SP 细胞被一个转变生长因素增加 --(TGF-) 导致了上皮间充质的转变(EMT ) ，并且这效果伴有 ABCG2 mRNA 表示，和减少的敏感的一条强壮的起来规定到 mitoxantrone。SP 房间在 TGF- 和房间的回复的移动之上被恢复到上皮的显型，并且 smad3 特定的 siRNA 响应 TGF- 减少了 SP 丰富。在结论， TGF -- 由 smad 依赖的发信号的小径的导致的 EMT 支持癌症开发和反癌症药由扩充许多 GBC-SD SP 房间的抵抗显型，和机制的更好的理解在 TGF 包含了 -- 导致的 EMT 可以为阻止癌症提供新奇策略前进。

英文摘要：

Mounting evidence has shown that side population （SP） cells are enriched for cancer stem cells （CSCs） responsible for cancer malignancy. In this study, SP technology was used to isolate a small subpopulation of SP cells in human gallbladder cancer cell line GBC-SD, and SP cells which had superior potential for proliferation in vitro and tumorigenesis in vivo were identified. Importantly, the abundance of GBC-SD SP cells was increased by a transforming growth factor-β （TGF-β）-induced epithelial-mesenchymal transition （EMT）, and this effect was accompanied with a strong up-regulation of ABCG2 mRNA expression, and a decreased sensitivity to mitoxantrone. SP cells were restored upon the removal of TGF-β and the reversion of the cells to an epithelial phenotype, and smad3-specific siRNA reduced SP abundance in response to TGF-β. In conclusion, TGF-β-induced EMT by smad-dependent signaling pathway promotes cancer development and anti-cancer drug resistant phenotype by augmenting the abundance of GBC-SD SP cells, and a better understanding of mechanisms involved in TGF-β-induced EMT may provide a novel strategy for preventing cancer progression.