UCA1 facilitates endometriosis progression through EIF4A3-mediated stabilization of E2F1 mRNA and enhanced glycolysis

Yingying Cao, Cao Y, Honglin Wang, Wang H, Gou Y, Yanling Gou, Huiyan Zhang, Zhang H, Jinming Liu, Liu J, Bai R, Rui Bai, Ruru Bai, Zongwen Liang, Liang Z, Zhao Y, Yuxin Zhao, Yu Zhao, Han X, Xu Han, Zongfeng Zhang, Zhang Z
Cellular signalling · 2026 · vol. 146 , pp. 112620 · doi:10.1016/j.cellsig.2026.112620 · PMID:42235624 · W7163149734
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

UCA1 promotes endometriosis progression by stabilizing E2F1 mRNA via EIF4A3, which subsequently enhances glycolysis.

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Abstract

Long non-coding RNA Urothelial carcinoma-associated 1 (UCA1) is a pivotal regulator in the progression of endometriosis (EMs), yet its mechanistic role remains elusive. This study identified UCA1 as a factor promoting glycolysis through bioinformatic screening and functional validation. Ectopic endometrial lesions exhibited significant UCA1 upregulation compared to normal endometrial tissues. In ectopic endometrial stromal cells, UCA1 knockdown suppressed glycolytic activity, evidenced by diminished glucose uptake and lactate production, while rescue experiments demonstrated that overexpression of E2F Transcription Factor 1 (E2F1) reversed this metabolic suppression. Mechanistically, UCA1 recruited eukaryotic translation initiation factor 4A3 (EIF4A3) to stabilize E2F1 mRNA, establishing an RNA-protein complex confirmed by RNA immunoprecipitation, RNA pull-down, and fluorescence in situ hybridization assays. Further experiments have demonstrated that EIF4A3 directly targets the 3'-untranslated region (UTR) of E2F1. Chromatin immunoprecipitation assays demonstrated that E2F1 binds to the promoter of pyruvate kinase isozyme type M2 (PKM2), thereby activating its transcription and linking UCA1-mediated E2F1 regulation to glycolytic reprogramming. In vivo validation using a subcutaneous xenograft model indicated that silencing UCA1 significantly inhibited the growth of endometriotic lesions. These findings support a UCA1/EIF4A3/E2F1/PKM2 regulatory axis that drives EMs progression through metabolic alterations. This study provides evidence for UCA1 as both a disease-promoting effector and a valuable therapeutic target, with implications for developing diagnostic and treatment strategies that target lncRNA-mediated metabolic dysregulation in EMs.

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Condition tags

endometriosis

MeSH descriptors

E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor E2F1 Transcription Factor

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (44)

SciLite annotations

chemicals 2
glucose lactate

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