CCN6在乳腺癌侵袭中的新作用

Cellscience Pub Date : 2009-10-01
Guadalupe Lorenzatti, Wei Huang, Celina G Kleer
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引用次数: 0

摘要

基质细胞蛋白CCN家族在细胞通讯和上皮间质交叉对话的调解中发挥重要作用,并在发育和癌症中发挥作用。特别是,CCN6信使RNA表达的缺失已经在高度侵袭性乳腺癌中得到确认,特别是在炎症性乳腺癌和伴有腋窝淋巴结转移的乳腺癌中。最近的研究结果可以更好地解释CCN6表达降低与人类浸润性乳腺癌的相关性。CCN6在上皮细胞向间充质转化(epithelial to mesenchymal transition, EMT)过程中发挥作用,将上皮细胞转化为具有侵袭能力的迁移间充质样细胞。虽然CCN6促进EMT和侵袭的机制尚未完全阐明,但目前的数据表明,它涉及将转录调节因子Snai1和ZEB1募集到E-cadherin启动子上。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The emerging role of CCN6 in breast cancer invasion.

The emerging role of CCN6 in breast cancer invasion.

The CCN family of matricellular proteins is essential for cell communication and mediation of epithelial stromal cross-talks with roles in development and cancer. In particular, loss of CCN6 messenger RNA expression has been recognized in highly aggressive breast cancers, especially in inflammatory breast cancer and breast cancers with axillary lymph node metastasis. Recent findings can better explain the relevance of CCN6's reduced expression on human invasive breast carcinomas. CCN6 has been shown to play a role in the process of epithelial to mesenchymal transition (EMT), which converts epithelial cells into migratory mesenchymal-like cells with invasive abilities. Although the mechanism by which CCN6 promotes EMT and invasion has not been fully elucidated, current data suggest that it involves the recruitment of the transcriptional regulators Snai1 and ZEB1 to the E-cadherin promoter.

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