The aim of this study was to explore how to modulate the expression of estrogen receptors (ER) α and β and to verify the role of ERα and β in relationship to estrogen and tamoxifen (TAM). A series of oligodeoxyribonucleotides (ODN) corresponding to regions of the ERα or β was tested in human endometrial cancer cell lines (HEC-1B). The change in HEC-1B proliferation in response to 17β-estradiol (E2) and TAM under the impact of antisense ODN was studied. The results of the study are as follows: 1) transfection with antisense ODN significantly inhibited ERα and ERβ protein production, 2) the cells lost the ability to proliferate in response to E2 after transfection with ERα antisense ODN especially at 24, 48, and 72 h. There was no obvious change in response to E2 in HEC-1B cell lines that were transfected with ERβ antisense ODN, and 3) after transfection with ERα antisense ODN, HEC-1B cells lost the ability to proliferate in response to TAM at 48 h. This inhibition was also observed after transfection with ERβ antisense ODN at 24 h. ERα may be the primary receptor in the proliferation of HEC-1B cells in response to E2. Both ERα and ERβ are involved in the agonist impact of TAM on endometrial cancer cells.
- antisense oligodeoxyribonucleotides
- endometrial carcinoma
- estrogen receptor
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