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[Study on the modulation of estrogen receptor isoforms alpha in endometrial carcinoma cells using antisense
Yan Zhang1, Qin-ping Liao, Li Yu
1Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing 100034, China.
Objective:
To verify the roles of estrogen receptor alpha in the tumogenesis of endometrial cancer in relationship with estrogen and tamoxifen, and to explore an efficient way to modulate the expression of estrogen receptor (ER) isoform alpha to built up a model of endometrial cancer cells expressing predominant one isoform of ERs for ultimately probing therapeutical and preventive antiestrogen for endometrial cancer.
Methods:
A series of oligodeoxyribonucleotides against regions of the human ERalpha was synthesized and tested in human endometrial cancer cell line (HEC-1B cells) that expressed functional ERalpha. The expressions of ER isoforms were detected by Western blot using specific antibody. The change of HEC-1B cell proliferation in response to 17beta-estradiol(E2) and tamoxifen(TAM) under the impact of antisense oligodeoxyribonucleotides (AS-ODN) was studied.
Results:
(1) Transfection with AS-ODN directed against the human ERalpha significantly inhibited ERalpha protein expression. (2) The proliferation of endometrial cancer cell line HEC-1B could be increased by both E(2) and TAM. The cells lost the ability to proliferate in response to E(2) after being transfected with ERalpha-AS-ODN at hours 24, 48 and 72. After being transfected with ERalpha-AS-ODN, HEC-1B cells lost the ability to proliferate in response to TAM at hour 48.
Conclusion:
(1) AS-ODNs directed against the human ERalpha can inhibit the expression of ER alpha effectively. The method can be used to built up a model of endometrial cancer cells expressing predominant one isoform of ERs. (2) ERalpha may be the primary receptor in the proliferation of HEC-1B cells in response to 17beta-estradiol and tamoxifen.
Insights
Antisense oligodeoxyribonucleotides effectively inhibit estrogen receptor alpha (ERalpha) expression in endometrial cancer cells. This inhibition blocks cell proliferation stimulated by estrogen and tamoxifen, suggesting ERalpha is key for tumor growth.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Context:
- Endometrial cancer is often driven by estrogen signaling.
- Estrogen receptor alpha (ERalpha) plays a crucial role in endometrial cancer development.
- Targeting ERalpha offers a potential therapeutic strategy.
Purpose:
- To investigate the role of ERalpha in endometrial cancer tumogenesis.
- To develop a method for modulating ERalpha expression in endometrial cancer cells.
- To create a cellular model for studying antiestrogen therapies.
Summary:
- Antisense oligodeoxyribonucleotides (AS-ODN) targeting ERalpha were synthesized and tested in HEC-1B endometrial cancer cells.
- AS-ODN transfection significantly reduced ERalpha protein expression.
- ERalpha inhibition abolished cell proliferation in response to 17beta-estradiol and tamoxifen.
Impact:
- AS-ODNs provide an effective means to inhibit ERalpha expression.
- This method allows for the creation of cell models with predominant ER isoforms.
- ERalpha is confirmed as a primary mediator of estrogen and tamoxifen-induced proliferation in HEC-1B cells.
