ArticleNeuro-oncology2022
RBBP4-p300 axis modulates expression of genes essential for cell survival and is a potential target for therapy in glioblastoma.
Article in Neuro-oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- G-CSF promotes H3K27ac-modified KLF5 to activate CXCR4 expression and drive colon cancer growth and metastasis.European journal of medical research · 2026Article
- Acetylation modification in malignant progression and therapeutic resistance of gliomas.Frontiers in cell and developmental biology · 2026Review
- Protein lactylation and immunotherapy in gliomas: A novel regulatory axis in tumor metabolism (Review).International journal of oncology · 2025Review
- Epigenetic regulation of histone modifications in glioblastoma: recent advances and therapeutic insights.Biomarker research · 2025Review
- The important role of the histone acetyltransferases p300/CBP in cancer and the promising anticancer effects of p300/CBP inhibitors.Cell biology and toxicology · 2025Review
- Old players and new insights: unraveling the role of RNA-binding proteins in brain tumors.Theranostics · 2025Review
- XPO1-inhibitor Selinexor induces MGMT expression by activating PKA-CREB signaling inFrontiers in oncology · 2025Article
- RBBP4: A novel diagnostic and prognostic biomarker for non-small-cell lung cancer correlated with autophagic cell death.Cancer medicine · 2024Article
- Interpreting the molecular mechanisms of RBBP4/7 and their roles in human diseases (Review).International journal of molecular medicine · 2024Review
- Bioinformatic and clinical experimental assay uncovers resistance and susceptibility mechanisms of human glioblastomas to temozolomide and identifies new combined and individual survival biomarkers outperformingTherapeutic advances in medical oncology · 2024Article
- KIF15 promotes human glioblastoma progression under the synergistic transactivation of REST and P300.International journal of biological sciences · 2024Article
- The Role of Non-Coding RNAs in Epigenetic Dysregulation in Glioblastoma Development.International journal of molecular sciences · 2023Review
- Effects of the Acetyltransferase p300 on Tumour Regulation from the Novel Perspective of Posttranslational Protein Modification.Biomolecules · 2023Review
- KATs off: Biomedical insights from lysine acetyltransferase inhibitors.Current opinion in chemical biology · 2023Review
- Unveiling the molecular structure and role of RBBP4/7: implications for epigenetic regulation and cancer research.Frontiers in molecular biosciences · 2023Review
- Epigenetic maintenance of the injury response state in glioblastoma stem cells.Neuro-oncology advancesArticle
- Pharmacologic inhibition of RBBP4/p300-mediated homologous recombination activity enhances glioblastoma sensitivity to temozolomide.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundRBBP4 activates transcription by histone acetylation, but the partner histone acetyltransferases are unknown. Thus, we investigated the hypothesis that RBBP4 interacts with p300 in a complex in glioblastoma (GBM).
methodsshRNA silencing of RBBP4 or p300 and RNAseq was used to identify genes co-regulated by RBBP4 and p300 in GBM43 patient-derived xenograft (PDX). RBBP4/p300 complex was demonstrated using proximity ligation assay (PLA) and ChIPseq delineated histone H3 acetylation and RBBP4/p300 complex binding in promoters/enhancers. Temozolomide (TMZ)-induced DNA double strand breaks (DSBs) were evaluated by γ-H2AX and proliferation by CyQuant and live cell monitoring assays. In vivo efficacy was based on survival of mice with orthotopic tumors.
resultsshRBBP4 and shp300 downregulated 4768 genes among which 1485 (31%) were commonly downregulated by both shRNAs, while upregulated genes were 2484, including 863 (35%) common genes. The pro-survival genes were the top-ranked among the downregulated genes, including C-MYC. RBBP4/p300 complex was demonstrated in the nucleus, and shRBBP4 or shp300 significantly sensitized GBM cells to TMZ compared to the control shNT in vitro (P < .05). Moreover, TMZ significantly prolonged the survival of mice bearing GBM22-shRBBP4 orthotopic tumors compared with control shNT tumors (median shNT survival 52 days vs. median shRBBP4 319 days; P = .001). CREB-binding protein (CBP)/p300 inhibitor CPI-1612 suppressed H3K27Ac and RBBP4/p300 complex target proteins, including C-MYC, and synergistically sensitized TMZ in vitro. Pharmacodynamic evaluation confirmed brain penetration by CPI-1612 supporting further investigation to evaluate efficacy to sensitize TMZ.
conclusionsRBBP4/p300 complex is present in GBM cells and is a potential therapeutic target.
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