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Published online
doi:10.1083/jcb.200809167
The Journal of Cell Biology, Vol. 185, No. 2, 203-211
The Rockefeller University Press, 0021-9525 $30.00
© Yuan et al.
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A c-Myc–SIRT1 feedback loop regulates cell growth and transformation



Jian Yuan, Katherine Minter-Dykhouse, and Zhenkun Lou

Division of Oncology Research, Department of Oncology, Mayo Clinic, Rochester, MN 55905

Correspondence to Zhenkun Lou: Lou.Zhenkun{at}mayo.edu

The protein deacetylase SIRT1 has been implicated in a variety of cellular functions, including development, cellular stress responses, and metabolism. Increasing evidence suggests that similar to its counterpart, Sir2, in yeast, Caenorhabditis elegans, and Drosophila melanogaster, SIRT1 may function to regulate life span in mammals. However, SIRT1's role in cancer is unclear. During our investigation of SIRT1, we found that c-Myc binds to the SIRT1 promoter and induces SIRT1 expression. However, SIRT1 interacts with and deacetylates c-Myc, resulting in decreased c-Myc stability. As a consequence, c-Myc's transformational capability is compromised in the presence of SIRT1. Overall, our experiments identify a c-Myc–SIRT1 feedback loop in the regulation of c-Myc activity and cellular transformation, supporting/suggesting a role of SIRT1 in tumor suppression.

Abbreviations used in this paper: ChIP, chromatin immunoprecipitation; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; LDHA, lactate dehydrogenase A; MEF, mouse embryonic fibroblast; mSHMT, mitochondrial serine hydroxymethyltransferase; QRT-PCR, quantitative RT-PCR; SBP, streptavidin-binding peptide; shRNA, short-hairpin RNA; TERT, telomerase reverse transcriptase gene; WT, wild type.

© 2009 Yuan et al.
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