Prohibitin2/PHB2, Transcriptionally Regulated by GABPA, Inhibits Cell Growth via PRKN/Parkin-dependent Mitophagy in Endometriosis
Prohibitin 2 (PHB2) is downregulated in endometriosis, where it inhibits cell growth via Parkin-mediated mitophagy, and its transcription is regulated by GABPA.
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The study investigated how prohibitin 2 (PHB2), transcriptionally regulated by GABPA, affects endometriosis by modulating PRKN/Parkin-dependent mitophagy and related cell behaviors. Using ectopic and normal ovarian endometrial tissues from patients with endometriosis, along with endometrial cell lines with PHB2 overexpression or knockdown, the authors measured PHB2 mRNA/protein levels and assessed proliferation, migration, invasion, apoptosis, and mitochondrial/autophagy/mitophagy marker changes. PHB2 was downregulated in ectopic endometrium, and restoring PHB2 inhibited proliferation, migration, and invasion while promoting apoptosis, alongside increased mitophagy markers (Parkin, LC3II/I) and decreased autophagy-related markers (P62, TOMM20), with GABPA identified as directly binding the PHB2 promoter to control its transcription. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.
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Cited by (4)
- Aberrant mitochondria in endometriosis: From pathogenic mechanisms to therapeutic opportunities 2026
- N-acetylcysteine stimulates organelle malfunction in endometriotic cells via IFN-gamma signaling 2025
- Erastin-induced multi-pathway cell death in endometriosis: a mechanistic and translational narrative review 2025
- Molecular mechanism of autophagy and apoptosis in endometriosis: Current understanding and future research directions 2024
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