ArticleNature communications2020
SPT6-driven error-free DNA repair safeguards genomic stability of glioblastoma cancer stem-like cells.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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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
21 citing papers in PubMed, 23 citations in OpenAlex.
- Metabolic Reprogramming in Glioblastoma Stem Cells Promotes Radiation Resistance Through a H3K18la/USP30/MBOAT2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular insights into DNA damage response plasticity in glioma stem cells.Communications biology · 2026Review
- FLASH Radiotherapy and Organelle-Targeted Radiosensitization in Glioblastoma: A Conceptual and Translational Review.Cancers · 2026Review
- FBXW7 Targets the SPT6-ΔNp63 Axis for Degradation to Inhibit Esophageal Tumorigenesis Induced by 4-Nitroquinoline N-Oxide.MedComm · 2026Article
- The interplay of DNA damage, epigenetics and tumour heterogeneity in driving cancer cell fitness.Nature communications · 2025Review
- Glioma stem cells: drivers of tumor progression and recurrence.Stem cell research & therapy · 2025Review
- Histone chaperones coupled to DNA replication and transcription control divergent chromatin elements to maintain cell fate.Genes & development · 2025Article
- Comparative Review on Cancer Pathology from Aberrant Histone Chaperone Activity.International journal of molecular sciences · 2024Review
- Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201.Neuro-oncology · 2024Article
- Transcriptional elongation control in developmental gene expression, aging, and disease.Molecular cell · 2023Review
- Insights into Spt6: a histone chaperone that functions in transcription, DNA replication, and genome stability.Trends in genetics : TIG · 2023Review
- The conserved histone chaperone Spt6 is strongly required for DNA replication and genome stability.Cell reports · 2023Article
- Review
- Review
- Cooperation between intrinsically disordered and ordered regions of Spt6 regulates nucleosome and Pol II CTD binding, and nucleosome assembly.Nucleic acids research · 2022Article
- BMI1 nuclear location is critical for RAD51-dependent response to replication stress and drives chemoresistance in breast cancer stem cells.Cell death & disease · 2022Article
- Beyond the Double-Strand Breaks: The Role of DNA Repair Proteins in Cancer Stem-Cell Regulation.Cancers · 2021Review
- EMP3 negatively modulates breast cancer cell DNA replication, DNA damage repair, and stem-like properties.Cell death & disease · 2021Article
- Targeted protein degradation reveals a direct role of SPT6 in RNAPII elongation and termination.Molecular cell · 2021Article
- The Identification of RNA-Binding Proteins Functionally Associated with Tumor Progression in Gastrointestinal Cancer.Cancers · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma cancer-stem like cells (GSCs) display marked resistance to ionizing radiation (IR), a standard of care for glioblastoma patients. Mechanisms underpinning radio-resistance of GSCs remain largely unknown. Chromatin state and the accessibility of DNA lesions to DNA repair machineries are crucial for the maintenance of genomic stability. Understanding the functional impact of chromatin remodeling on DNA repair in GSCs may lay the foundation for advancing the efficacy of radio-sensitizing therapies. Here, we present the results of a high-content siRNA microscopy screen, revealing the transcriptional elongation factor SPT6 to be critical for the genomic stability and self-renewal of GSCs. Mechanistically, SPT6 transcriptionally up-regulates BRCA1 and thereby drives an error-free DNA repair in GSCs. SPT6 loss impairs the self-renewal, genomic stability and tumor initiating capacity of GSCs. Collectively, our results provide mechanistic insights into how SPT6 regulates DNA repair and identify SPT6 as a putative therapeutic target in glioblastoma.
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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.