The aim of this study was to investigate the expression and distribution of estrogen receptor (ER)α, ERβ, G-protein-coupled ER-1 (GPER), androgen receptor (AR), progesterone receptor (PR)A, PRB and connective tissue growth factor (CTGF) in the vaginal wall among women who had been treated for cervical cancer with radiotherapy.
Interestingly, Raloxifene-a GPER-activating selective estrogen receptor modulator-has recently been demonstrated to be preventive for cervical cancer relapse in mice.
Together, these data suggest that E2-mediated ERα signalling is critical for the sustenance of FOXP3 expression and T<sub>reg</sub> cell function in human CxCa via direct interaction of ERα with FOXP3 promoter.
Estrogen receptor α and PRB were mainly expressed in the stroma but not in the carcinoma tissues of the cervical cancer, and their expressions were highly correlated.
Significantly, despite clinical, epidemiological, and animal model results linking estrogen and estrogen receptor alpha (ERα) to CxCa, ERα expression declined >15-fold from normalcy to cancer, showing the strongest inverse correlation of any gene with the increasing expression of p16, a marker for HPV-linked cancers.
The aim of the present study was to investigate ESR1 promoter methylation in cervical cancer and correlate methylation status with clinico-pathological parameters.
In the current study, we investigated whether estrogen receptor alpha (ERalpha) is required for the development of cervical cancer in K14E7 transgenic mice.