Interaction between HSP60 and β-catenin promotes metastasis
2009; Oxford University Press; Volume: 30; Issue: 6 Linguagem: Inglês
10.1093/carcin/bgp087
ISSN1460-2180
AutoresYa-Ping Tsai, Muh‐Hwa Yang, Chi-Hung Huang, Shyue‐Yih Chang, Po‐Min Chen, Chung‐Ji Liu, Shu‐Chun Teng, Kou-Juey Wu,
Tópico(s)Galectins and Cancer Biology
ResumoHeat 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.
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