Abstract：
:Tumor-associated mutants of the p53 tumor suppressor protein exert biological activities compatible with an oncogenic gain of function. To explore the underlying molecular mechanism, we performed microarray analysis, comparing p53-null cells to mutant p53-expressing cells. One of the genes up-regulated in the presence of mutant p53 was EGR1, a transcription factor implicated in growth control, apoptosis, and cancer. EGR1 induction by various types of stress is markedly augmented in cells expressing mutant p53. Moreover, chromatin immunoprecipitation analysis indicates that mutant p53 is physically associated with the EGR1 promoter. Functional assays indicate that induction of EGR1 by mutant p53 contributes to enhanced transformed properties and resistance to apoptosis. We propose that EGR1 is a significant contributor to mutant p53 gain of function.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Weisz L,Zalcenstein A,Stambolsky P,Cohen Y,Goldfinger N,Oren M,Rotter Vdoi
10.1158/0008-5472.CAN-04-1145subject
Has Abstractpub_date
2004-11-15 00:00:00pages
8318-27issue
22eissn
0008-5472issn
1538-7445pii
64/22/8318journal_volume
64pub_type
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