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“替代” EMT 开关。

The 'alternative' EMT switch.

机构信息

Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK.

出版信息

Breast Cancer Res. 2011 Aug 16;13(4):313. doi: 10.1186/bcr2915.

DOI:10.1186/bcr2915
PMID:21884643
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3236334/
Abstract

Epithelial to mesenchymal transition (EMT) is an essential process in embryonic development and is aberrantly induced in many disease settings. Work carried out by Chonghui Cheng's laboratory addressed the involvement of alternative RNA splicing in EMT and its link to tumour progression. They describe a switch in CD44 expression from variant isoform(s) to the standard isoform and showed, for the first time, that this is required for normal epithelial cells to undergo EMT. In addition, they link expression of the CD44 standard isoform with high-grade breast cancer and to activation of the phosphoinositide 3-kinase/Akt pathway and apoptosis resistance in a mouse model of recurrent disease.

摘要

上皮-间充质转化(EMT)是胚胎发育过程中的一个重要过程,在许多疾病状态下异常诱导。Chonghui Cheng 实验室的工作涉及到选择性 RNA 剪接在 EMT 中的参与及其与肿瘤进展的联系。他们描述了 CD44 表达从变异异构体向标准异构体的转变,并首次表明这是正常上皮细胞发生 EMT 所必需的。此外,他们还将 CD44 标准异构体的表达与高级别乳腺癌以及磷酸肌醇 3-激酶/ Akt 通路的激活和复发性疾病小鼠模型中的凋亡抵抗联系起来。

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CD44/CD44v6 a Reliable Companion in Cancer-Initiating Cell Maintenance and Tumor Progression.CD44/CD44v6:癌症起始细胞维持和肿瘤进展中的可靠“伙伴”
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本文引用的文献

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CD44 splice isoform switching in human and mouse epithelium is essential for epithelial-mesenchymal transition and breast cancer progression.CD44 剪接异构体转换在人及小鼠上皮组织中对于上皮-间质转化和乳腺癌进展是必需的。
J Clin Invest. 2011 Mar;121(3):1064-74. doi: 10.1172/JCI44540.
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CD44: can a cancer-initiating cell profit from an abundantly expressed molecule?CD44:一个高表达的分子能使癌症起始细胞获益吗?
Nat Rev Cancer. 2011 Apr;11(4):254-67. doi: 10.1038/nrc3023. Epub 2011 Mar 10.
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Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged.癌症中替代前体 mRNA 剪接调控:脱节的通路和程序。
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Podoplanin associates with CD44 to promote directional cell migration.足突蛋白与 CD44 结合促进定向细胞迁移。
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An ESRP-regulated splicing programme is abrogated during the epithelial-mesenchymal transition.ESRP 调控的剪接程序在上皮-间充质转化过程中被废除。
EMBO J. 2010 Oct 6;29(19):3286-300. doi: 10.1038/emboj.2010.195. Epub 2010 Aug 13.
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Tumor necrosis factor-alpha regulates transforming growth factor-beta-dependent epithelial-mesenchymal transition by promoting hyaluronan-CD44-moesin interaction.肿瘤坏死因子-α通过促进透明质酸-CD44-肌动蛋白结合促进转化生长因子-β依赖性上皮间质转化。
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Cell. 2009 Nov 25;139(5):871-90. doi: 10.1016/j.cell.2009.11.007.
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ESRP1 and ESRP2 are epithelial cell-type-specific regulators of FGFR2 splicing.ESRP1和ESRP2是FGFR2剪接的上皮细胞类型特异性调节因子。
Mol Cell. 2009 Mar 13;33(5):591-601. doi: 10.1016/j.molcel.2009.01.025.
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The epithelial-mesenchymal transition generates cells with properties of stem cells.上皮-间质转化产生具有干细胞特性的细胞。
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