Tumor suppressor p53 maintains genome stability by regulating diverse cellular functions including
cell cycle arrest, apoptosis, senescence and metabolic homeostasis. Mutations in the p53 gene occur in almost
all human cancers with a frequency of up to 80%. However, it is only 20% in breast cancers, 18% in
endometrial cancers and 1.5% in cervical cancers. Estrogen receptor alpha (ERα) plays a pivotal role in
hormone-dependent cancer development and the status of ERα is used for designing treatment strategy and
for prognosis. A closer look at the cross-talk between p53 and ERα has revealed that their activities are
mutually regulated. This review will summarize the current body of knowledge on p53, ERα and ERβ in cancer.
Clinical correlations between estrogen receptors and p53 status have also been reported. Thus, this review will
discuss the relationship between p53 and ERs at both the molecular and clinical levels.