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miR-200c 在上皮-间充质转化、抗细胞凋亡和乳腺癌干细胞表型的交汇点。

miR-200c at the nexus of epithelial-mesenchymal transition, resistance to apoptosis, and the breast cancer stem cell phenotype.

出版信息

Breast Cancer Res. 2011 Jun 10;13(3):110. doi: 10.1186/bcr2885.

DOI:10.1186/bcr2885
PMID:21682933
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3218941/
Abstract

Decreased expression of miRNAs of the miR-200 family has been implicated in the growth and metastasis of breast cancer cells. Of this family, miR-200c has garnered particular attention as a consequence of its ability to target ZEB1 and ZEB2, mediators of epithelial- mesenchymal transition. An article in the previous issue of Breast Cancer Research identifies additional targets of miR-200c that link increased cancer cell invasiveness, resistance to apoptosis, and induction of breast cancer stem cell characteristics.

摘要

miR-200 家族的 miRNA 表达降低与乳腺癌细胞的生长和转移有关。在这个家族中，miR-200c 因其能够靶向上皮-间充质转化的调节因子 ZEB1 和 ZEB2 而备受关注。上一期的《乳腺癌研究》杂志上的一篇文章确定了 miR-200c 的其他靶标，这些靶标与增加癌细胞侵袭性、抗细胞凋亡以及诱导乳腺癌干细胞特性有关。

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本文引用的文献

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2
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Oncogene. 2011 Sep 1;30(35):3735-44. doi: 10.1038/onc.2011.96. Epub 2011 Apr 11.
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Loss of miR-200 inhibition of Suz12 leads to polycomb-mediated repression required for the formation and maintenance of cancer stem cells.miR-200 抑制 Suz12 的丧失导致多梳介导的抑制，这是癌症干细胞形成和维持所必需的。
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miR-200c regulates induction of apoptosis through CD95 by targeting FAP-1.miR-200c 通过靶向 FAP-1 调控 CD95 诱导细胞凋亡。
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microRNAs and EMT in mammary cells and breast cancer.微小 RNA 与 EMT 在乳腺细胞和乳腺癌中的作用。
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The EMT-activator ZEB1 promotes tumorigenicity by repressing stemness-inhibiting microRNAs.EMT激活因子ZEB1通过抑制抑制干性的微小RNA来促进肿瘤发生。
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