Setdb1, a novel interactor of ΔNp63, is involved in breast tumorigenesis
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Carla Regina1, Mirco Compagnone1, Angelo Peschiaroli2, AnnaMaria Lena1, Margherita Annicchiarico-Petruzzelli3, Maria Cristina Piro1, Gerry Melino1, Eleonora Candi1,3
1Department of Experimental Medicine and Surgery, University of Rome “Tor Vergata”, Rome, Italy
2CNR, Institute of Cell Biology and Neurobiology (IBCN), Rome, Italy
3IDI-IRCCS, Rome, Italy
Eleonora Candi, email: firstname.lastname@example.org
Keywords: p63, SETDB1, breast cancer, histone methyl transferase, proliferation
Received: August 21, 2015 Accepted: January 13, 2016 Published: January 31, 2016
ΔNp63 has been recently involved in self-renewal potential of breast cancer stem cells. Although the p63 transcriptional profile has been extensively characterized, our knowledge of the p63-binding partners potentially involved in the regulation of breast tumour progression is limited. Here, we performed the yeast two hybrid approach to identify p63α interactors involved in breast tumorigenesis and we found that SETDB1, a histone lysine methyl transferases, interacts with ΔNp63α and that this interaction contributes to p63 protein stability. SETDB1 is often amplified in primary breast tumours, and its depletion confers to breast cancer cells growth disadvantage. We identified a list of thirty genes repressed by ΔNp63 in a SETDB1-dependent manner, whose expression is positively correlated to survival of breast cancer patients. These results suggest that p63 and SETDB1 expression, together with the repressed genes, may have diagnostic and prognostic potential.
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