ArticleNucleic acids research2020
Long noncoding RNA HCP5 participates in premature ovarian insufficiency by transcriptionally regulating MSH5 and DNA damage repair via YB1.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 121 citations in OpenAlex.
- Bioengineering Ovarian Endocrine Function: From Follicle Modeling to Cell-Based Hormone Therapy.Advanced healthcare materials · 2026Review
- Oocyte-specific knockout of eIF2B subunits causes apoptosis of mouse oocytes within the early growing follicles via DNA damage and mitochondrial dysfunction.Cell death & disease · 2026Article
- 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
- Oocyte-specific knockout of eIF2 subunits causes apoptosis of mouse oocytes within the early growing follicles via mitochondrial dysfunctions and DNA damage.Cell death & disease · 2026Article
- Exosome-transmitted long noncoding RNA SNHG1 promotes prostate cancer bone metastasis via YBX1/MMP16 axis.Cell death discovery · 2026Article
- Methyltransferase-Like 3 Inhibition-Activated cGAS/STING Axis Enhances Immunotherapy and Poly(ADP-Ribose) Polymerase Inhibitor Sensitivity in Lung Adenocarcinoma.Research (Washington, D.C.) · 2026Article
- Statistical methods to disentangle genetic effects influencing infertility and early fetal viability with a genome-wide application.PLoS genetics · 2025Article
- Identification of lncRNA expression profiles associated with ovarian development and ageing process in mice.Journal of applied genetics · 2025Article
- The implications of LncRNAs and premature ovarian insufficiency.Journal of ovarian research · 2025Review
- Stress granule clearance mediated by V-ATPase-interacting protein NCOA7 mitigates ovarian aging.Nature aging · 2025Article
- Downregulation of FOXO1 in PCOS Granulosa Cells: A Direct Target of microRNA-183.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- The risk factors, pathogenesis and treatment of premature ovarian insufficiency.Journal of ovarian research · 2025Review
- Non-coding RNA-mediated granulosa cell dysfunction during ovarian aging: From mechanisms to potential interventions.Non-coding RNA research · 2025Review
- Aberrant downregulation of Y-box binding protein 1 expression impairs the cell cycle in an mCellular and molecular life sciences : CMLS · 2025Article
- Mitigating chemotherapy-induced granulosa cell damage: role of hUCMSC-EVs in regulating the lncRNA HCP5-miR-20a-5p-YAP1 network.Cell biology and toxicology · 2025Article
- SLC30A4-AS1 Mediates the Senescence of Periodontal Ligament Stem Cells in Inflammatory Environments via the Alternative Splicing of TP53BP1.Cell proliferation · 2025Article
- Sustained release of miR-21 carried by mesenchymal stem cell-derived exosomes from GelMA microspheres inhibits ovarian granulosa cell apoptosis in premature ovarian insufficiency.Materials today. Bio · 2025Article
- GMRSP encoded by lncRNA H19 regulates metabolic reprogramming and alleviates aortic dissection.Nature communications · 2025Article
- Analysis of post-transcriptional regulatory signatures and immune cell subsets in premature ovarian insufficiency based on full-length transcriptome.Scientific reports · 2025Article
- Long non-coding RNA-encoded micropeptides: functions, mechanisms and implications.Cell death discovery · 2024Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetic etiology of premature ovarian insufficiency (POI) has been well established to date, however, the role of long noncoding RNAs (lncRNAs) in POI is largely unknown. In this study, we identified a down-expressed lncRNA HCP5 in granulosa cells (GCs) from biochemical POI (bPOI) patients, which impaired DNA damage repair and promoted apoptosis of GCs. Mechanistically, we discovered that HCP5 stabilized the interaction between YB1 and its partner ILF2, which could mediate YB1 transferring into the nucleus of GCs. HCP5 silencing affected the localization of YB1 into nucleus and reduced the binding of YB1 to the promoter of MSH5 gene, thereby diminishing MSH5 expression. Taken together, we identified that the decreased expression of HCP5 in bPOI contributed to dysfunctional GCs by regulating MSH5 transcription and DNA damage repair via the interaction with YB1, providing a novel epigenetic mechanism for POI pathogenesis.
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