ArticleInternational journal of oral science2025
NUP62 alleviates senescence and promotes the stemness of human dental pulp stem cells via NSD2-dependent epigenetic reprogramming.
Article in International journal of oral science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Mesenchymal stem/stromal cell senescence in aging and regenerative medicine: a systematic review.Biogerontology · 2026Review
- NUP62 Elevates USP10 Expression and Promotes Tamoxifen Resistance of Breast Cancer by Deubiquitinating ERα.Annals of surgical oncology · 2026Article
- Review
- The role of HMGA1 in genome stability: Implications in human cancer.Cellular and molecular life sciences : CMLS · 2026Review
- NUP85 as a Pan-Cancer Immune Biomarker: Integrated Multi Omics and Functional Analyses Reveal Its Role in Tumor Prognosis.ImmunoTargets and therapy · 2026Article
- Post-translational modifications in the oral microenvironment: Stem cell regulation from periodontal regeneration to oral cancer therapy.World journal of stem cells · 2025Review
- USP5-Laden ApoEVs and E2F1 Stabilization in Disc Repair: Unresolved Questions on Senescence, Specificity and Endosomal Escape.Journal of extracellular vesicles · 2025Article
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Authors and funding
14 authors.
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Abstract
Stem cells play a crucial role in maintaining tissue regenerative capacity and homeostasis. However, mechanisms associated with stem cell senescence require further investigation. In this study, we conducted a proteomic analysis of human dental pulp stem cells (HDPSCs) obtained from individuals of various ages. Our findings showed that the expression of NUP62 was decreased in aged HDPSCs. We discovered that NUP62 alleviated senescence-associated phenotypes and enhanced differentiation potential both in vitro and in vivo. Conversely, the knocking down of NUP62 expression aggravated the senescence-associated phenotypes and impaired the proliferation and migration capacity of HDPSCs. Through RNA-sequence and decoding the epigenomic landscapes remodeled induced by NUP62 overexpression, we found that NUP62 helps alleviate senescence in HDPSCs by enhancing the nuclear transport of the transcription factor E2F1. This, in turn, stimulates the transcription of the epigenetic enzyme NSD2. Finally, the overexpression of NUP62 influences the H3K36me2 and H3K36me3 modifications of anti-aging genes (HMGA1, HMGA2, and SIRT6). Our results demonstrated that NUP62 regulates the fate of HDPSCs via NSD2-dependent epigenetic reprogramming.
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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 OpenQuestion graph.