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[Cancer Research 64, 8318-8327, November 15, 2004]
© 2004 American Association for Cancer Research

Regular Articles

Transactivation of the EGR1 Gene Contributes to Mutant p53 Gain of Function

Lilach Weisz, Amir Zalcenstein, Perry Stambolsky, Yehudit Cohen, Naomi Goldfinger, Moshe Oren and Varda Rotter

Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel

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.




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Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
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