Premium
SIRT 2‐mediated inactivation of p73 is required for glioblastoma tumorigenicity
Author(s) -
Funato Kosuke,
Hayashi Tomoatsu,
Echizen Kanae,
Negishi Lumi,
Shimizu Naomi,
KoyamaNasu Ryo,
NasuNishimura Yukiko,
Morishita Yasuyuki,
Tabar Viviane,
Todo Tomoki,
Ino Yasushi,
Mukasa Akitake,
Saito Nobuhito,
Akiyama Tetsu
Publication year - 2018
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201745587
Subject(s) - glioblastoma , cancer research , chemistry , biology , microbiology and biotechnology
Glioblastoma is one of the most aggressive forms of cancers and has a poor prognosis. Genomewide analyses have revealed that a set of core signaling pathways, the p53, RB , and RTK pathways, are commonly deregulated in glioblastomas. However, the molecular mechanisms underlying the tumorigenicity of glioblastoma are not fully understood. Here, we show that the lysine deacetylase SIRT 2 is required for the proliferation and tumorigenicity of glioblastoma cells, including glioblastoma stem cells. Furthermore, we demonstrate that SIRT 2 regulates p73 transcriptional activity by deacetylation of its C‐terminal lysine residues. Our results suggest that SIRT 2‐mediated inactivation of p73 is critical for the proliferation and tumorigenicity of glioblastoma cells and that SIRT 2 may be a promising molecular target for the therapy of glioblastoma.