Premium
A member of the ETS family, EHF, and the ATPase RUVBL1 inhibit p53‐mediated apoptosis
Author(s) -
Taniue Kenzui,
Oda Takeaki,
Hayashi Tomoatsu,
Okuno Masumi,
Akiyama Tetsu
Publication year - 2011
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 - 10.1038/embor.2011.81
Subject(s) - biology , histone , chromatin , cancer research , microbiology and biotechnology , apoptosis , transcription factor , hek 293 cells , gene , genetics
Tumour cells are known to be dependent on, or ‘addicted to’, not only oncogenes, but also some non‐oncogenes. However, the mechanisms by which tumour cells are addicted to these genes have not been fully explained. Here, we show that overexpression of a member of the ETS family, EHF, is required for the survival of colon tumour cells that contain wild‐type p53. We found that EHF directly activates the transcription of RUVBL1 , an ATPase associated with chromatin‐remodelling complexes. RUVBL1 blocks p53‐mediated apoptosis by repressing the expression of p53 and its target genes. Moreover, we found that RUVBL1 represses p53 transcription by binding to the p53 promoter, interfering with RNF20/hBRE1‐mediated histone H2B monoubiquitination and promoting PAF1‐mediated histone H3K9 trimethylation. These results indicate that EHF‐mediated RUVBL1 expression allows colon tumour cells to avoid p53‐mediated apoptosis. Thus, EHF and RUVBL1 might be promising molecular targets for the treatment of colon tumours.