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Effect of AT1R knockdown on ishikawa cell proliferation induced by estrogen
Qing Yang1, Qing Su, Guangwei Wang
1Department of Obstetrics and Gynecology, Shengjing Hospital, China Medical University, Shen Yang 110004, China. Yangq@sj-hospital.org
Objective:
This study aimed to study the effects of angiotensin receptor (AT1R) on proliferation, cell cycle progression, and apoptosis of estrogen-induced ishikawa cell by the transfection of AT1R-siRNA.
Methods:
Immunofluorescence method was used to detect AT1R in ishikawa cell. Western blot was used to detect the expression of AT1R protein in ishikawa cell before and after the transfection of AT1R-siRNA. MTT method was used to test the cell proliferation of estrogen-induced ishikawa cell before and after the transfection. Western blot was used to detect the expression of extracellular regulated protein kinase1/2(ERK1/2).
Results:
The result of immunofluorescence shows that AT1R was expressed in ishikawa cell. The expression of AT1R protein was inhibited obviously by 72 h after the transfection of AT1R-siRNA. The results of MTT show that estrogen could induce the cell proliferation of ishikawa cell. The expression of ERK1/2 was down-regulated after the transfection of AT1R-siRNA.
Conclusion:
AT1R can promote the cell proliferation of estrogen-induced ishikawa cell. The possible mechanism may be down-regulating the expression of ERK1/2 protein.
Insights
Angiotensin receptor (AT1R) promotes estrogen-induced Ishikawa cell proliferation. Inhibiting AT1R down-regulates extracellular regulated protein kinase 1/2 (ERK1/2) expression, suggesting a potential therapeutic target.
Area of Science:
- Gynecology
- Molecular Biology
- Cell Biology
Background:
- Estrogen plays a role in Ishikawa cell proliferation.
- Angiotensin receptor (AT1R) involvement in gynecological cancers requires further investigation.
Purpose of the Study:
- To investigate the effect of AT1R on estrogen-induced Ishikawa cell proliferation, cell cycle, and apoptosis.
- To explore the mechanism by which AT1R influences these processes.
Main Methods:
- Immunofluorescence and Western blot were used to detect AT1R expression.
- AT1R-siRNA transfection was employed to inhibit AT1R.
- MTT assays assessed cell proliferation.
- Western blot analyzed extracellular regulated protein kinase 1/2 (ERK1/2) expression.
Main Results:
- AT1R was detected in Ishikawa cells.
- AT1R-siRNA transfection significantly inhibited AT1R protein expression within 72 hours.
- Estrogen induced Ishikawa cell proliferation.
- AT1R inhibition led to down-regulation of ERK1/2 expression.
Conclusions:
- AT1R promotes proliferation in estrogen-induced Ishikawa cells.
- The mechanism may involve the down-regulation of ERK1/2 protein expression.
- Targeting AT1R could be a potential strategy for managing related gynecological conditions.
