Direct regulation of HSP60 expression by c-MYC induces transformation.
The c-MYC proto-oncogene encodes a ubiquitous transcription factor involved in cell proliferation and tumorigenesis. 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 cancer. Here we show that c-MYC directly activates HSP60 transcription through an E-box (CACGTG) site located in the proximal promoter of the HSP60 gene. Overexpression of HSP60 induces transformation. Short-interference RNA (siRNA) mediated repression of HSP60 reduces transformation caused by c-MYC overexpression. These results indicate that c-MYC may promote transformation through the induction of HSP60 expression.
Tsai
Ya-Ping
YP
Institute of Biochemistry and Molecular Biology, National Yang-Ming University, No. 115, Li-Nong St., Peitou, Taipei 112, Taiwan.
Teng
Shu-Chun
SC
Wu
Kou-Juey
KJ
D000818:Animals; D045744:Cell Line, Tumor; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D018834:Chaperonin 60 / Q000235:genetics*; D024721:E-Box Elements; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D000090063:Proto-Oncogene Mas; D020598:Proto-Oncogene Proteins c-myb / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D051381:Rats; D014158:Transcription, Genetic
D018834:Chaperonin 60; C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D020598:Proto-Oncogene Proteins c-myb