CIHR Group in Skeletal Development and Remodeling, Division of Oral Biology and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Dental Sciences Building, University of Western Ontario, London, ON, N6A 5C1, Canada,
J Cell Commun Signal. 2008 Jun;2(1-2):47-8. doi: 10.1007/s12079-008-0027-1. Epub 2008 Sep 3.
The YAP transcription coactivator has been implicated as an oncogene and is amplified in human cancers. Previously, it has been shown that CCN2 (connective tissue growth factor, CTGF) is a target of the tumor promoting YAP and its transcription factor target TEAD. A recent report in Genes and Development by Zhao and colleagues (Genes Dev 22:1962-1971 2008) has extended these initial observations to show that CCN2 plays an important role in the growth-promoting function of YAP. These data confirm the role of CCN2 as a key oncogenic mediator. This report briefly summarizes these findings.
YAP 转录共激活因子已被认为是一种致癌基因，并在人类癌症中扩增。此前已经表明，CCN2（结缔组织生长因子，CTGF）是促进肿瘤的 YAP 及其转录因子靶标 TEAD 的靶标。最近，Zhao 及其同事在《基因与发育》（Genes Dev 22:1962-1971 2008）上的一篇报道扩展了这些初步观察结果，表明 CCN2 在 YAP 的促生长功能中发挥重要作用。这些数据证实了 CCN2 作为关键致癌介质的作用。本报告简要总结了这些发现。
