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Journal of Chongqing Medical University ; (12)2007.
Article in Chinese | WPRIM | ID: wpr-581311

ABSTRACT

Objective:To explore the mechanisms of ERK in affecting estrogen receptor signaling pathway by investigating the changes of the expression levels of nuclear receptor co-activatorPCAF protein and wild-type P53 protein and their gene transcription in the process of estrogen promoting transformation of cell cycle and resisting apoptosis of breast cancer cell MCF-7 after inhibitting ERK. Methods:Estrogen receptor-positive breast cancer cells MCF-7 were divided into 17?-estradiol treatment group,17 ?-E2 + ERK inhibitor PD98059 treatment group,and the control group. The apoptosis of cell and cycle were analyzed by flow cytometry. The expression of phosphorylated ERK1/2 and PCAF protein and wild-type p53 were detected by Western blot.The expression of pcaf mRNA and wild-type p53 mRNA were detected by RT-PCR. Results:With phosphorylation inhibitor of ERK PD98059,the effect of 17?-estradiol in resisting apoptosis and prmoting transformation of MCF-7 cell cycle was reversed,and the rate of early apoptosis of MCF-7 cell was raised(P0.05).The protein expression level and gene transcription of wild-type P53 were reinforced (P

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