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 17β-estradiol treatment group

17 β-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 17β-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(P<0.05).The numberof G1 phase cells increased

and the numberof S and Mphase cells decreased(P <0.01). The expression level of PCAF protein and P-ERK1/2 protein decreased remarkably (P<0.01). The difference ofgene transcription ofPCAF had no statistical significance(P>0.05).The protein expression level and gene transcription of wild-type P53 were reinforced (P<0.01 ). Conclusion:The effect of ERK on estrogen in resisting apoptosis and promoting transformation of breast cancercell MCF-7 are associated with PCAF enhancing the signal of estrogen receptor

and changing of the expression level of wild-type p53 protein and its gene transcription.