Back Cover: The PES1/FOXM1 heterodimer suppresses TCF21 and ERβ expression in ovarian endometriosis (View 1/2024)

Jingwen Zhu, Peili Wu, Ruihui Lu, Cheng Zeng, Chao Peng, Yingfang Zhou, Qing Xue
In: VIEW · 2024 · vol. 5(1) · doi:10.1002/viw2.341 · W4391847915
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-08 ⓘ

The PES1/FOXM1 heterodimer was identified as a regulator that suppresses the expression of TCF21 and ERβ in ovarian endometriosis.

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⚙ AI-generated deep summary by qwen3.7-flash, 2026-08-20 · read from full text ⓘ

This study investigates the molecular mechanisms underlying ovarian endometriosis by examining the roles of transcription factor 21 (TCF21) and estrogen receptor beta (ERβ). The researchers found that the PES1/FOXM1 heterodimer suppresses the expression of these key factors, with PES1 specifically reducing FOXM1 protein stability and weakening its inhibitory effect on TCF21 and ERβ. Experimental models demonstrated that overexpressing PES1 effectively suppressed the growth of ectopic lesions in mice, highlighting its potential as a therapeutic target. This paper is centrally about endometriosis — specifically the regulation of lesion growth via the PES1/FOXM1 pathway in ovarian endometriosis.

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Back Cover: The PES1/FOXM1 heterodimer suppresses TCF21 and ERβ expression in ovarian endometriosis (View 1/2024) Graphical Abstract In article number 20230090, Qing Xue and her co-workers have display that transcription factor 21 (TCF21) and estrogen receptor beta (ERβ, encoded by ESR2) are the key factors in the pathogenesis of endometriosis, but their co-regulation mechanism is still unknown. PES1 is downregulated in ectopic lesions. PES1 reduces the stability of the FOXM1 protein and weakens the transcriptional inhibition of ERβ and TCF21 by FOXM1. Overexpression of PES1 could effectively suppress the growth of ectopic lesions in mice indicating that PES1 has therapeutic potential for endometriosis.

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endometriosis

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last seen: 2026-06-10T17:14:06.276822+00:00
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