Journal Article

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 and Kou-Juey Wu

in Carcinogenesis

Volume 30, issue 6, pages 1049-1057
Published in print June 2009 | ISSN: 0143-3334
Published online April 2009 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgp087
Interaction between HSP60 and β-catenin promotes metastasis

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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.

Journal Article.  6040 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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