Lorenzatti Guadalupe, Huang Wei, Kleer Celina G
CIBICI-CONICET, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina.
Dept. of Pathology & Comprehensive Cancer Center, University of Michigan Medical School, USA.
Cellscience. 2009 Oct;6(2):146-157.
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.
CCN 家族的基质细胞蛋白对于细胞通讯以及上皮-间质相互作用的介导至关重要，在发育和癌症中发挥作用。特别是，在侵袭性很强的乳腺癌中，尤其是在炎性乳腺癌和伴有腋窝淋巴结转移的乳腺癌中，已发现 CCN6 信使核糖核酸表达缺失。最近的研究结果能更好地解释 CCN6 表达降低与人类浸润性乳腺癌的相关性。CCN6 已被证明在上皮-间质转化（EMT）过程中发挥作用，该过程将上皮细胞转化为具有侵袭能力的迁移性间充质样细胞。尽管 CCN6 促进 EMT 和侵袭的机制尚未完全阐明，但目前的数据表明，这涉及将转录调节因子 Snai1 和 ZEB1 招募到 E-钙黏蛋白启动子。
