HSP 60 overexpression increases the protein levels of the p110α subunit of phosphoinositide 3‐kinase and c‐Myc
FQ Yan, JQ Wang, YP Tsai… - Clinical and Experimental …, 2015 - Wiley Online Library
FQ Yan, JQ Wang, YP Tsai, KJ Wu
Clinical and Experimental Pharmacology and Physiology, 2015•Wiley Online LibrarySummary Heat shock protein 60 (HSP 60) is a chaperone protein which plays an essential
role in facilitating the folding of many newly synthesized proteins to reach their native forms.
Increased HSP 60 expression is observed in various types of human cancers. However,
proteins induced by HSP 60 to mediate transformation remain largely unknown. Here we
show that HSP 60 overexpression increases the protein levels of the p110α subunit of
phosphoinositide 3‐kinase (PI 3K). The amino acid domain 288‐383 of HSP 60 is used to …
role in facilitating the folding of many newly synthesized proteins to reach their native forms.
Increased HSP 60 expression is observed in various types of human cancers. However,
proteins induced by HSP 60 to mediate transformation remain largely unknown. Here we
show that HSP 60 overexpression increases the protein levels of the p110α subunit of
phosphoinositide 3‐kinase (PI 3K). The amino acid domain 288‐383 of HSP 60 is used to …
Summary
Heat shock protein 60 (HSP60) is a chaperone protein which plays an essential role in facilitating the folding of many newly synthesized proteins to reach their native forms. Increased HSP60 expression is observed in various types of human cancers. However, proteins induced by HSP60 to mediate transformation remain largely unknown. Here we show that HSP60 overexpression increases the protein levels of the p110α subunit of phosphoinositide 3‐kinase (PI3K). The amino acid domain 288‐383 of HSP60 is used to increase the protein levels. Overexpression of HSP60 also induces the levels of phosphorylated Akt. In addition, the amino acid domain 288‐383 of HSP60 is used to induce c‐Myc expression. Finally, a mono‐ubiquitinated form of β‐catenin has a higher activity to activate β‐catenin downstream targets compared to wild‐type β‐catenin. These results indicate that HSP60 overexpression induces the levels or activity of multiple oncogenic proteins to mediate transformation.
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