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by claude@2026-06, 2026-06-10
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Increased SUMOylation of TCF21 in endometriotic cells, enhanced by estrogen, improves its stability and interaction with USF2, boosting SF-1 and ERβ promoter activity and ESC proliferation.
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by claude@2026-06, 2026-06-10
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This study examined how posttranslational SUMOylation regulates transcription factor 21 (TCF21) in human ovarian endometriosis, using comparisons between endometriotic and eutopic tissues and stromal cells, as well as estrogen stimulation and inhibitor experiments. The authors found increased SUMOylated TCF21 levels in endometriotic tissues and stromal cells, with estrogen enhancing this modification; inhibiting SUMOylation with ginkgolic acid and assessing protein half-life indicated that SUMOylation stabilizes TCF21. Co-immunoprecipitation suggested SUMOylation increases TCF21’s interaction with USF2, and promoter binding assays showed that SUMOylation enhances USF2 binding to SF-1 and ERβ promoters; SUMOylation motifs also affected endometriotic stromal cell proliferation. This paper is centrally about endometriosis — it specifically investigates how increased TCF21 SUMOylation stabilizes and increases TCF21-driven SF-1/ERβ regulation in human endometriotic stromal cells.
Abstract
Endometriosis is an estrogen-dependent disease. Our previous study demonstrated that elevated levels of transcription factor 21 (TCF21) in endometriotic tissues enhanced steroidogenic factor-1 (SF-1) and estrogen receptor β (ERβ) expression by forming a heterodimer with upstream stimulatory factor 2 (USF2), allowing these TCF21/USF2 complexes to bind to the promoters of SF-1 and ERβ. Furthermore, TCF21 contributed to the increased proliferation of endometriotic stromal cells (ESCs), suggesting that TCF21 may play a vital role in the pathogenesis of endometriosis. SUMOylation is a posttranslational modification that has emerged as a crucial molecular regulatory mechanism. However, the mechanism regulating TCF21 SUMOylation in endometriosis is incompletely characterized. Thus, this study aimed to explore the effect of TCF21 SUMOylation on its expression and regulation in ovarian endometriosis. We found that the levels of SUMOylated TCF21 were increased in endometriotic tissues and stromal cells compared with eutopic endometrial tissues and stromal cells and enhanced by estrogen. Treatment with the SUMOylation inhibitor ginkgolic acid and the results of a protein half-life assay demonstrated that SUMOylation can stabilize the TCF21 protein. A coimmunoprecipitation assay showed that SUMOylation probably increased its interaction with USF2. Further analyses elucidated that SUMOylation of TCF21 significantly increased the binding activity of USF2 to the SF-1 and ERβ promoters. Moreover, the SUMOylation motifs in TCF21 affected the proliferation ability of ESCs. The results of this study suggest that SUMOylation plays a critical role in mediating the high expression of TCF21 in ESCs and may participate in the development of endometriosis.
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Increased SUMOylation of TCF21 improves its stability and function in human endometriotic stromal cells
- Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing 100034, China
Endometriosis is an estrogen-dependent disease. Our previous study demonstrated that elevated levels of transcription factor 21 (TCF21) in endometriotic tissues enhanced steroidogenic factor-1 (SF-1) and estrogen receptor β (ERβ) expression by forming a heterodimer with upstream stimulatory factor 2 (USF2), allowing these TCF21/USF2 complexes to bind to the promoters of SF-1 and ERβ. Furthermore, TCF21 contributed to the increased proliferation of endometriotic stromal cells (ESCs), suggesting that TCF21 may play a vital role in the pathogenesis of endometriosis. SUMOylation is a posttranslational modification that has emerged as a crucial molecular regulatory mechanism. However, the mechanism regulating TCF21 SUMOylation in endometriosis is incompletely characterized. Thus, this study aimed to explore the effect of TCF21 SUMOylation on its expression and regulation in ovarian endometriosis. We found that the levels of SUMOylated TCF21 were increased in endometriotic tissues and stromal cells compared with eutopic endometrial tissues and stromal cells and enhanced by estrogen. Treatment with the SUMOylation inhibitor ginkgolic acid (GA) and the results of a protein half-life assay demonstrated that SUMOylation can stabilize the TCF21 protein. A coimmunoprecipitation (Co-IP) assay showed that SUMOylation probably increased its interaction with USF2. Further analyses elucidated that SUMOylation of TCF21 significantly increased the binding activity of USF2 to the SF-1 and ERβ promoters. Moreover, the SUMOylation motifs in TCF21 affected the proliferation ability of ESCs. The results of this study suggest that SUMOylation plays a critical role in mediating the high expression of TCF21 in ESCs and may participate in the development of endometriosis.
- Sponsoring Organization:
- USDOE
- OSTI ID:
- 1770451
- Journal Information:
- Biology of Reproduction, Journal Name: Biology of Reproduction; ISSN 0006-3363
- Publisher:
- Oxford University PressCopyright Statement
- Country of Publication:
- United States
- Language:
- English
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