Interaction between HSP60 and β-catenin promotes metastasis

Ya Ping Tsai, Muh Hwa Yang, Chi Hung Huang, Shyue Yih Chang, Po Min Chen, Chung Ji Liu, Shu Chun Teng, Kou Juey Wu*

*此作品的通信作者

研究成果: Article同行評審

106 引文 斯高帕斯(Scopus)

摘要

Heat shock protein 60 (HSP60) plays an essential role in assisting many newly synthesized proteins to reach their native forms. Increased HSP60 expression is observed in different types of human cancers with metastasis (e.g. pancreatic cancer and large bowel carcinoma). However, the role of HSP60 in metastasis remains little known. Aberrant activation of β-catenin plays a key role in tumorigenesis and metastasis. Here, we show that overexpression of HSP60 induces metastatic phenotypes in vitro and in vivo. HSP60 interacts with β-catenin, increases β-catenin protein levels through the apical domain and enhances its transcriptional activity. Short-interference RNA-mediated repression of β-catenin reverts metastatic activity caused by HSP60 overexpression. Proteosomal activity is not required for the induction of β-catenin by HSP60. Coexpression of HSP60 and nuclear β-catenin predicts a worse prognosis of metastatic head and neck cancer patients. These results implicate a novel role of HSP60 in metastasis.

原文English
頁(從 - 到)1049-1057
頁數9
期刊Carcinogenesis
30
發行號6
DOIs
出版狀態Published - 2009

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