ArticleGenes & development2013
Widespread resetting of DNA methylation in glioblastoma-initiating cells suppresses malignant cellular behavior in a lineage-dependent manner.
Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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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.
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Who cites it
92 citing papers in PubMed, 137 citations in OpenAlex.
- Article
- Human iPSC-derived and conventional cancer models in precision oncology: advancing patient-specific therapies from bench to bedside.Journal of experimental & clinical cancer research : CR · 2026Review
- Disruption of the NDC80-Nek2 axis suppresses glioblastoma stemness and enhances therapeutic efficacy.Journal of translational medicine · 2026Article
- Direct transdifferentiation of tumorigenic melanoma cells induces tumor cell reversion.Cell death & disease · 2025Article
- Knockdown of Anoikis-Associated Gene OCIAD2 Reduces Proliferation and Migration of Glioblastoma Cell Lines.Combinatorial chemistry & high throughput screening · 2025Article
- Cyclin F-EXO1 axis controls cell cycle-dependent execution of double-strand break repair.Science advances · 2024Article
- Possible Strategies to Reduce the Tumorigenic Risk of Reprogrammed Normal and Cancer Cells.International journal of molecular sciences · 2024Review
- Role of hydroxymethylglutharyl-coenzyme A reductase in the induction of stem-like states in breast cancer.Journal of cancer research and clinical oncology · 2024Article
- Reprogramming and multi-lineage transdifferentiation attenuate the tumorigenicity of colorectal cancer cells.The Journal of biological chemistry · 2024Article
- Expression of calpastatin hcast 3-25 and activity of the calpain/calpastatin system in human glioblastoma stem cells: possible involvement of hcast 3-25 in cell differentiation.Frontiers in molecular biosciences · 2024Article
- Proteomic profiling of centrosomes across multiple mammalian cell and tissue types by an affinity capture method.Developmental cell · 2023Article
- Application of Induced Pluripotent Stem Cells in Malignant Solid Tumors.Stem cell reviews and reports · 2023Review
- Redox Homeostasis and Beyond: The Role of Wild-Type Isocitrate Dehydrogenases for the Pathogenesis of Glioblastoma.Antioxidants & redox signaling · 2023Review
- Connecting the dots: Melanoma cell of origin, tumor cell plasticity, trans-differentiation, and drug resistance.Pigment cell & melanoma research · 2023Review
- Restricting epigenetic activity promotes the reprogramming of transformed cells to pluripotency in a line-specific manner.Cell death discovery · 2023Article
- Modeling brain and neural crest neoplasms with human pluripotent stem cells.Neuro-oncology · 2023Review
- Merits and challenges of iPSC-derived organoids for clinical applications.Frontiers in cell and developmental biology · 2023Review
- Review
- Cell Fate Reprogramming in the Era of Cancer Immunotherapy.Frontiers in immunology · 2021Review
- Future Match Making: When Pediatric Oncology Meets Organoid Technology.Frontiers in cell and developmental biology · 2021Review
32 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 8 institutions in 6 countries.
Funding
Abstract
Epigenetic changes are frequently observed in cancer. However, their role in establishing or sustaining the malignant state has been difficult to determine due to the lack of experimental tools that enable resetting of epigenetic abnormalities. To address this, we applied induced pluripotent stem cell (iPSC) reprogramming techniques to invoke widespread epigenetic resetting of glioblastoma (GBM)-derived neural stem (GNS) cells. GBM iPSCs (GiPSCs) were subsequently redifferentiated to the neural lineage to assess the impact of cancer-specific epigenetic abnormalities on tumorigenicity. GiPSCs and their differentiating derivatives display widespread resetting of common GBM-associated changes, such as DNA hypermethylation of promoter regions of the cell motility regulator TES (testis-derived transcript), the tumor suppressor cyclin-dependent kinase inhibitor 1C (CDKN1C; p57KIP2), and many polycomb-repressive complex 2 (PRC2) target genes (e.g., SFRP2). Surprisingly, despite such global epigenetic reconfiguration, GiPSC-derived neural progenitors remained highly malignant upon xenotransplantation. Only when GiPSCs were directed to nonneural cell types did we observe sustained expression of reactivated tumor suppressors and reduced infiltrative behavior. These data suggest that imposing an epigenome associated with an alternative developmental lineage can suppress malignant behavior. However, in the context of the neural lineage, widespread resetting of GBM-associated epigenetic abnormalities is not sufficient to override the cancer genome.
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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.