The tumor suppressor p53 is a negative regulator of estrogen receptor signaling pathways.
The estrogen receptor (ER) is a ligand-dependent transcription factor which regulates growth, development, differentiation and reproduction. To test the hypothesis that the diverse effects of the ER could be mediated by interacting with other transcription factors/oncogenes, the present study assessed its interaction with the tumor suppressor p53. p53 is a transcription factor which is involved in cell cycle regulation and apoptosis. We found that the wild-type p53 physically interacted with ER in vivo and repressed the estrogen-activated transcriptional activity. However, p53 mutants had no or reduced repression effect, depending on the sites of mutation. These findings suggest that p53 can cross talk with the ER in hormone-activated signaling pathways in cells.
Yu
C L
CL
Division of Basic Sciences, National Institute of Child Health and Development, National Cancer Institute, Bethesda 20892-4255, Maryland, USA.
Driggers
P
P
Barrera-Hernandez
G
G
Nunez
S B
SB
Segars
J H
JH
Cheng
S
S
D016889:Endometrial Neoplasms; D005260:Female; D016147:Genes, Tumor Suppressor; D006801:Humans; D009154:Mutation; D011960:Receptors, Estrogen / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D014158:Transcription, Genetic; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
D011960:Receptors, Estrogen; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53