ArticleGenes & development2013
Genome-wide RNAi screens in human brain tumor isolates reveal a novel viability requirement for PHF5A.
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.
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.
The trial behind it
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Who cites it
92 citing papers in PubMed, 153 citations in OpenAlex.
- Modeling gliomas with organoids: Classification, fidelity, and guidelines for translational neuro-oncology.Neuro-oncology · 2026Review
- Deciphering Shared Gene Signatures and Immune Infiltration Characteristics Between Gestational Diabetes Mellitus and Preeclampsia by Integrated Bioinformatics Analysis and Machine Learning.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- KAT5 regulates neurodevelopmental states associated with G0-like populations in glioblastoma.Nature communications · 2025Article
- Splicing control by PHF5A is crucial for melanoma cell survival.Cell proliferation · 2025Article
- CLK2 Condensates Reorganize Nuclear Speckles and Induce Intron Retention.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- PHF5A promotes esophageal squamous cell carcinoma progression via stabilizing VEGFA.Biology direct · 2024Article
- ELISL: early-late integrated synthetic lethality prediction in cancer.Bioinformatics (Oxford, England) · 2024Article
- PHF5A is a potential diagnostic, prognostic, and immunological biomarker in pan-cancer.Scientific reports · 2023Article
- KMT2A associates with PHF5A-PHF14-HMG20A-RAI1 subcomplex in pancreatic cancer stem cells and epigenetically regulates their characteristics.Nature communications · 2023Article
- PHF5A regulates the expression of the DOCK5 variant to promote HNSCC progression through p38 MAPK activation.Biology direct · 2023Article
- PHF5A as a new OncoTarget and therapeutic prospects.Heliyon · 2023Review
- Delineating the glioblastoma stemness by genes involved in cytoskeletal rearrangements and metabolic alterations.World journal of stem cells · 2023Review
- WDR5 represents a therapeutically exploitable target for cancer stem cells in glioblastoma.Genes & development · 2023Article
- [PHF5A Promotes Proliferation and Migration of Non-Small Cell Lung Cancer by Regulating of PI3K/AKT Pathway].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Article
- PHF5A facilitates the development and progression of gastric cancer through SKP2-mediated stabilization of FOS.Journal of translational medicine · 2023Article
- A comprehensive pan-cancer analysis unveiling the oncogenic effect of plant homeodomain finger protein 14 (PHF14) in human tumors.Frontiers in genetics · 2023Article
- Research progress and therapeutic prospect of PHF5A acting as a new target for malignant tumors.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Review
- Article
- The mutation in splicing factor genes correlates with unfavorable prognosis, genomic instability, anti-tumor immunosuppression and increased immunotherapy response in pan-cancer.Frontiers in cell and developmental biology · 2022Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
Abstract
To identify key regulators of human brain tumor maintenance and initiation, we performed multiple genome-wide RNAi screens in patient-derived glioblastoma multiforme (GBM) stem cells (GSCs). These screens identified the plant homeodomain (PHD)-finger domain protein PHF5A as differentially required for GSC expansion, as compared with untransformed neural stem cells (NSCs) and fibroblasts. Given PHF5A's known involvement in facilitating interactions between the U2 snRNP complex and ATP-dependent helicases, we examined cancer-specific roles in RNA splicing. We found that in GSCs, but not untransformed controls, PHF5A facilitates recognition of exons with unusual C-rich 3' splice sites in thousands of essential genes. PHF5A knockdown in GSCs, but not untransformed NSCs, astrocytes, or fibroblasts, inhibited splicing of these genes, leading to cell cycle arrest and loss of viability. Notably, pharmacologic inhibition of U2 snRNP activity phenocopied PHF5A knockdown in GSCs and also in NSCs or fibroblasts overexpressing MYC. Furthermore, PHF5A inhibition compromised GSC tumor formation in vivo and inhibited growth of established GBM patient-derived xenograft tumors. Our results demonstrate a novel viability requirement for PHF5A to maintain proper exon recognition in brain tumor-initiating cells and may provide new inroads for novel anti-GBM therapeutic strategies.
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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.