Coppari group discovers key molecular mechanisms suppressing cancer stemness

The group of Roberto Coppari recently published the article “SIRT6 Suppresses Cancer Stem-like Capacity in Tumors with PI3K Activation Independently of Its Deacetylase Activity” in the Journal Cell Reports. The study characterized a key mechanism suppressing cancer stemness, involving the histone deacetylase sirtuin 6 or SIRT6. The Coppari lab has been interested for many years in cancer stem cells and their high tumorigenic capacity. In the present study, the team, led by the PhD student Rafael Maciel Ioris and by the postdoctoral researcher Giorgio Ramadori and Mirco Gallie, shows that overexpression of SIRT6 reduces growth, progression, and grade of breast cancer in a mouse model with phosphatidylinositol-3-kinase (or PI3K) activation. In fact, the researchers found that SIRT6 overexpression causes metabolic rearrangements in this cancer model by inhibiting PI3K signaling and stem-like characteristics. This work involved a wide range of techniques and the collaboration of several research teams. The group of Pierre Baldi, working at the Department of Computer Science University of California, Irvine, was involved in the transcriptomic and metabolomic analyses of this study. Moreover, the group of Raul Mostoslavsky at Harvard Medical School and MIT in Boston, helped with Chormatin Immunoprecipitaion assays. Altogether, the results obtained help to understand better the mechanisms underlying cancer stemness, they may place SIRT6 as a putative molecular target for new therapies to eradicate the disease. 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Posted by: S. Ljubicic

 

 

 

 

22 March 2017

PHYM News

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