ArticleAmerican journal of translational research2017
GSK3β activity is essential for senescence-associated heterochromatin foci (SAHF) formation induced by HMGA2 in WI38 cells.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
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- High glucose promotes atherosclerosis by regulating miRNA let7d-5p level.Journal of diabetes investigation · 2024Article
- Senescence-Associated Heterochromatin Foci Suppress γ-H2AX Focus Formation Induced by Radiation Exposure.International journal of molecular sciences · 2024Article
- The role of high mobility group proteins in cellular senescence mechanisms.Frontiers in aging · 2024Review
- ZIM1 Combined with Hydrogel Inhibits Senescence of Primary PαS Cells during In Vitro Expansion.International journal of molecular sciences · 2023Article
- The functional impact of nuclear reorganization in cellular senescence.Briefings in functional genomics · 2022Review
- Targeting NUFIP1 Suppresses Growth and Induces Senescence of Colorectal Cancer Cells.Frontiers in oncology · 2021Article
- High Mobility Group AT-Hook 2 (HMGA2) Oncogenicity in Mesenchymal and Epithelial Neoplasia.International journal of molecular sciences · 2020Review
- MCMV triggers ROS/NLRP3-associated inflammasome activation in the inner ear of mice and cultured spiral ganglion neurons, contributing to sensorineural hearing loss.International journal of molecular medicine · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is an irreversible form of cell cycle arrest, which is often characterized by domains of facultative heterochromatin substructures also known as senescence-associated heterochromatin foci (SAHF). SAHF assembly is likely mediated through the downregulation of the Wnt pathway, which inhibits Glycogen Synthase Kinase 3 Beta (GSK3β) in cells undergoing replicative senescence. Alternatively, High Mobility Group AT-Hook 2 (HMGA2) can also induce SAHF formation in primary cells, through a process in which the involved cell signaling pathway is unknown. Accordingly, it is important to determine whether GSK3β and the Wnt pathway are necessary during HMGA2-induced SAHF formation. In this study, we developed a senescence model for SAHF assembly in WI38 cell through ectopic expression of HMGA2. In this model, typical senescent features were identified, including elevated SA-β-galactosidase staining and the downregulation of the Wnt pathway. We also showed that the GSK3β inhibitor LiCl can partly disable SAHF formation through the HMGA2 overexpression in WI38 cells. However, the disabled SAHF formation resulting from the inactivity of GSK3β in our senescence model cannot be restored through ectopic overexpression of Catenin Beta 1 (
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28123643PMC5250713W2584193275What OpenQuestion holds
Registered trials
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