ArticleCell biology and toxicology2025
Mitigating chemotherapy-induced granulosa cell damage: role of hUCMSC-EVs in regulating the lncRNA HCP5-miR-20a-5p-YAP1 network.
Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Immediate protective effect of rUCMSC-EVs on ovarian function in a cyclophosphamide -induced premature ovarian insufficiency rats: counteracting granulosa cell apoptosis.Journal of ovarian research · 2026Article
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The substantial apprehension facing young cancer patients revolves around the onset of chemotherapy-induced premature ovarian failure (POF), primarily linked to damage inflicted upon granulosa cells (GCs). The inquiry delves into the protective role of extracellular vesicles (EVs) derived from human umbilical cord mesenchymal stem cells (hUCMSCs) in mitigating chemotherapy-induced ovarian failure. Specifically, we investigated the mechanism by which hUCMSC-EVs deliver the long non-coding RNA (lncRNA) HCP5 to regulate DNA damage repair in GCs via the miR-20a-5p/YAP1 axis. The detection of differentially expressed lncRNAs in GC injury resulting from cyclophosphamide (CP) was conducted through transcriptome sequencing. hUCMSC-EVs were isolated, characterized, and co-cultured with CP-injured GCs. Functional assays such as CCK-8, TUNEL, and ELISA were performed to evaluate GC viability, apoptosis, and ovarian endocrine function. Experimental validation of the interactions involving HCP5, miR-20a-5p, and YAP1 was achieved through performing luciferase reporter assays, RNA immunoprecipitation experiments, and Western blot (WB) analyses. HCP5 was significantly enriched in hUCMSC-EVs and effectively delivered into GCs. This resulted in improved GC viability, reduced apoptosis, and enhanced DNA repair. Mechanistically, HCP5 sponged miR-20a-5p, leading to the upregulation of YAP1, which in turn mitigated CP-induced GC damage. In vivo experiments further demonstrated that hUCMSC-EVs prevented CP-induced POF through modulation of the HCP5-miR-20a-5p-YAP1 axis. Our research underscores the therapeutic potential of hUCMSC-EVs in delivering HCP5 to promote DNA repair in GCs, thereby preventing chemotherapy-induced POF. This study provides a novel molecular framework for future therapeutic strategies aimed at protecting ovarian function during chemotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.