Phenotypic plasticity and epithelial-mesenchymal transitions in cancer and normal stem cells?
Phenotypic plasticity and epithelial-mesenchymal transitions in cancer and normal stem cells?
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DOI：
10.1002/ijc.26311
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发表时间：
2011-11-15
影响因子：
6.4
通讯作者：
Weinberg, Robert A.
中科院分区：
文献类型：
--
作者：
Scheel, Christina;Weinberg, Robert A.
关键词：
癌症干细胞（CSCs）在自我更新能力和产生大量分化程度更高的后代方面与正常干细胞相似。与被认为是正常组织内稳态的普遍模式的等级组织相反，表型可塑性允许癌细胞动态地进入和退出干细胞状态。上皮-间质转化（Epithelial-Mesenchymal Transition， EMT）与癌细胞侵袭性和干细胞特性的获得密切相关。因此，EMT程序成为癌症细胞表型可塑性的重要调节因子，包括它们进入干细胞状态。关于EMT在癌细胞中通过表观遗传机制的调控以及EMT程序对正常组织稳态的贡献，还有很多需要了解的。
Cancer stem cells (CSCs) are similar to normal stem cells in their ability to self-renew and to generate large populations of more differentiated descendants. In contrast to the hierarchical organization that is presumed to be the prevalent mode of normal tissue homeostasis, phenotypic plasticity allows cancer cells to dynamically enter into and exit from stem-cell states. The Epithelial-Mesenchymal Transition (EMT) has been closely associated with the acquisition of both invasive and stem-cell properties in cancer cells. Thereby, EMT programs emerge as important regulators of phenotypic plasticity in cancer cells including their entrance into stem-cell states. Much is still to be learned about the regulation of EMTs through epigenetic mechanisms in cancer cells and the contributions that EMT programs make to normal tissue homeostasis.
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DOI：
10.1126/science.1180794
发表时间：
2010-01-29
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Li L;Clevers H
通讯作者：
Clevers H
影响因子：
64.8
作者：
O'Brien, Catherine A.;Pollett, Aaron;Dick, John E.
通讯作者：
Dick, John E.
影响因子：
11.5
作者：
O'Brien, Catherine Adell;Kreso, Antonija;Jamieson, Catriona H. M.
通讯作者：
Jamieson, Catriona H. M.
影响因子：
64.8
作者：
Quintana, Elsa;Shackleton, Mark;Sabel, Michael S.;Fullen, Douglas R.;Johnson, Timothy M.;Morrison, Sean J.
通讯作者：
Morrison, Sean J.
影响因子：
64.5
作者：
Gupta PB;Onder TT;Jiang G;Tao K;Kuperwasser C;Weinberg RA;Lander ES
通讯作者：
Lander ES