Abstract
The protein deacetylase SIRT1 has been implicated in a variety of cellular functions, including development, cellular stress response, and metabolism. Increasing evidence suggests that similar to the roles of its counterpart in low organisms (Sir2), SIRT1 may regulate life span regulation in higher organisms. During our investigation of SIRT1 regulation, we found that c-Myc could bind to SIRT1 promoter and induce SIRT1 expression. On the other hand, we found that SIRT1 interacts with c-Myc and deacetylates c-Myc, resulting in decreased c-Myc stability. As a consequence, c-Myc\#8217;s transformational capability becomes compromised in the presence of SIRT1. Overall, our studies identify a c-Myc-SIRT1 feedback loop in the regulation of c-Myc activity and cellular transformation, supporting a role of SIRT1 in tumor suppression.
Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 4441.
100th AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO