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Altered claudin-4 expression in progesterone-treated endometrial adenocarcinoma cell line Ishikawa
Pan Xiao-Yu1, Jin Yan, Feng Cui-Ping
1Department of Obstetrics and Gynecology, China-Japan Friendship Hospital, Beijing, People's Republic of China. changpanxiaoyu@163.com
Objective:
To detect the expression change of claudin-4 in Ishikawa endometrial adenocarcinoma cell line in response to progesterone. To determine whether claudin-4 is involved in the anticancer effect of progesterone.
Methods:
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to determine the 50% inhibitory concentration (IC50) of megestrol acetate (MA) in treating Ishikawa cells. After the Ishikawa cells were treated with MA at IC50, cell apoptosis was examined by flow cytometry and transmission electron microscopy. The messenger RNA and protein expression levels of claudin-4 were further quantified by real-time polymerase chain reaction and Western blot. The localization of claudin-4 was examined by immunofluorescent staining.
Results:
The IC50 of MA on Ishikawa cells was 15 mg/L incubated for 72 hours. Apoptosis percentage was elevated from 0.07% ± 0.02% to 3.93% ± 0.81% after MA treatment. The expression of claudin-4 at both protein and messenger RNA levels was significantly decreased after the treatment of MA (P < 0.05). The localization of claudin-4 transferred from cytomembrane to cytoplasm and nucleus.
Conclusion:
Megestrol acetate can inhibit the growth of Ishikawa cells. It may work through decreasing claudin-4 expression and cell apoptosis. The localization change of claudin-4 may also be involved in the anticancer effect of progesterone.
Insights
Progesterone, via megestrol acetate, inhibits endometrial cancer cell growth by decreasing claudin-4 expression and inducing apoptosis. Claudin-4
Area of Science:
- Endocrinology
- Molecular Biology
- Cancer Research
Background:
- Endometrial adenocarcinoma is a significant health concern.
- Progesterone is a key hormone with potential anticancer effects.
- Claudin-4's role in endometrial cancer is not fully understood.
Purpose of the Study:
- To investigate the effect of progesterone on claudin-4 expression in Ishikawa endometrial adenocarcinoma cells.
- To determine if claudin-4 is involved in the anticancer mechanisms of progesterone.
Main Methods:
- Ishikawa cells were treated with megestrol acetate (MA) at its IC50.
- Cell viability was assessed using MTT assay.
- Apoptosis was analyzed by flow cytometry and transmission electron microscopy.
- Claudin-4 mRNA and protein levels were quantified using RT-PCR and Western blot.
- Claudin-4 localization was visualized by immunofluorescent staining.
Main Results:
- Megestrol acetate (MA) inhibited Ishikawa cell growth with an IC50 of 15 mg/L.
- MA treatment significantly increased apoptosis from 0.07% to 3.93%.
- Both mRNA and protein expression of claudin-4 were significantly reduced post-MA treatment.
- Claudin-4 shifted from the cell membrane to the cytoplasm and nucleus.
Conclusions:
- Megestrol acetate effectively inhibits endometrial adenocarcinoma cell growth.
- The anticancer effect may involve decreased claudin-4 expression and induced apoptosis.
- Progesterone's role in endometrial cancer may be mediated by claudin-4 expression and localization changes.
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