Send to

Choose Destination
See comment in PubMed Commons below
Med Hypotheses. 2006;67(2):341-4. Epub 2006 Mar 20.

SIRT1: tumor promoter or tumor suppressor?

Author information

Department of Biochemistry, Fralin Biotechnology Center, Virginia Tech, West Campus Drive, Blacksburg, VA 24061, USA.


Over the past decade, an intensive research on the basic biology of aging has identified individual genes either directly or indirectly involved in regulating the aging process in various model organisms. This allows us to garner all the information available from studies of model organisms and to apply them to better understand aging and cancer in human. Among many genes thus far reported contributing to aging process, the yeast silent information regulator-2 (SIR2) and its homologues in other species, which belong to the family of type III histone and protein deacetylases, have been the subject of active discussion. The demonstrated roles of SIRT1, the mammalian counterpart of the yeast SIR2, reveal that SIRT1 regulates important cellular processes including anti-apoptosis, neuronal protection, cellular senescence, aging and longevity. Based on the observations that SIRT1 is upregulated in tumor cells, the hypothesis is that deregulation of SIRT1 expression may promote tumorigenesis by altering cellular signaling or by inducing modulation of chromatin remodeling leading to promotion of tumorigenesis. Further studies will shed new light on the underlying mechanisms of tumorigenesis mediated by SIRT1.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center