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TGF-β/snail-mediated epithelial-to-mesenchymal transition disrupts estradiol metabolism through suppressing the
Ping Jin1, Jinxuan Cai2, Na Chen3
1Shenzhen Maternity and Child Healthcare Hospital, Shenzhen, Guangdong, 518055, China; The First School of Clinical Medicine, Southern Medical University, Shenzhen, Guangdong, 518055, China.
Abstract:
Endometriosis affects nearly 10 % of reproductive-age women and is characterized by the growth of endometrial-like tissues outside the uterus. This disease poses significant diagnostic and therapeutic challenges due to its unknown origins and complex pathophysiology. Our study investigates how epithelial-mesenchymal transition (EMT) contributes to the dysregulation of estradiol metabolism by suppressing hydroxysteroid 17β dehydrogenase 2 (HSD17B2) expression in endometriotic epithelial cells. We used Gene Set Variation Analysis (GSVA) on public microarray data to correlate EMT scores with HSD17B2 levels. This approach revealed a significant correlation, showing that EMT is linked to reduced HSD17B2 expression in endometriotic tissues. Furthermore, our qPCR and immunoblotting results showed that TGF-β-induced EMT significantly reduced HSD17B2 expression in human endometriotic 12Z epithelial cells. Additionally, our data showed that Snail, an EMT-related transcription factor, acts on the E-box motif in the HSD17B2 promoter to suppress transcription. Our findings show that EMT is associated with decreased HSD17B2 expression in endometriotic tissues. This downregulation disrupts estradiol metabolism, possibly contributing to endometriosis pathogenesis. Our study offers critical insights into the molecular mechanisms of endometriosis and suggests that targeting EMT, especially the TGF-β/Snail axis, could provide a new therapeutic approach.
Insights
Epithelial-mesenchymal transition (EMT) reduces HSD17B2 expression in endometriosis, disrupting estradiol metabolism. Targeting the TGF-β/Snail pathway may offer new endometriosis therapies.
Area of Science:
- Reproductive biology
- Molecular endocrinology
- Cellular signaling
Background:
- Endometriosis affects 10% of women, presenting diagnostic and therapeutic challenges.
- Its complex pathophysiology and unknown origins necessitate deeper molecular investigation.
- Epithelial-mesenchymal transition (EMT) is implicated in various fibrotic diseases.
Purpose of the Study:
- To investigate the role of EMT in regulating estradiol metabolism in endometriosis.
- To explore the impact of EMT on hydroxysteroid 17β dehydrogenase 2 (HSD17B2) expression.
- To identify potential therapeutic targets within the EMT pathway.
Main Methods:
- Gene Set Variation Analysis (GSVA) on public microarray data to correlate EMT scores with HSD17B2 levels.
- Quantitative PCR (qPCR) and immunoblotting to assess HSD17B2 expression in response to TGF-β.
- Analysis of Snail transcription factor binding to the HSD17B2 promoter.
Main Results:
- A significant negative correlation between EMT scores and HSD17B2 levels in endometriotic tissues.
- TGF-β-induced EMT significantly decreased HSD17B2 expression in human endometriotic cells.
- Snail directly suppresses HSD17B2 transcription via its promoter region.
Conclusions:
- EMT is associated with decreased HSD17B2 expression in endometriosis, disrupting local estradiol metabolism.
- The TGF-β/Snail signaling pathway plays a key role in this downregulation.
- Targeting EMT, particularly the TGF-β/Snail axis, represents a promising therapeutic strategy for endometriosis.
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