ArticleCancer cell2024
Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer.
Article in Cancer cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Positive selection screen identifies natural product β-catenin inactivators.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- BRD9 Degraders Unleash GBAF Chromatin Remodeling Activity in Synovial Sarcoma.Cancer research · 2026Article
- Integrating molecular subtypes, genomics and functional dependencies to identify context-specific therapeutic vulnerabilities in small cell lung cancer.Biomarker research · 2026Review
- Probing Centromere Plasticity and Chromatin Remodeling Using Single-Molecule Techniques.Cell biology international · 2026Review
- Targeting Tex10 Overcomes Oxaliplatin Resistance by Competitively Disrupting the Non-Canonical BAF Complex in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transcriptional evidence of neuroendocrine cell plasticity beyond histological boundaries in lung neuroendocrine neoplasms: an in-silico analysis suggesting a progression model.Journal of experimental & clinical cancer research : CR · 2026Article
- Oncogenic Gα signaling requires AP-3-dependent recruitment to the endolysosomal compartment.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Next-generation sequencing elucidates the distinct mutational landscape of SMARCA4-deficient lung cancer.Oncology letters · 2026Article
- SMARCD1 and Its Functional Relevance in SWI/SNF and Cancer.International journal of molecular sciences · 2026Review
- Vascular STING activation facilitates NK cell anti-tumor immunity in small cell lung cancer.Cancer cell · 2026Article
- Transcription Factor Subtype Governs Response and Resistance to DLL3-Directed T-Cell Engagement in Small Cell Lung Cancer.bioRxiv : the preprint server for biology · 2026Article
- A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.Science (New York, N.Y.) · 2026Article
- Subtype-specific dependencies and therapeutic opportunities in small cell lung cancer.Science advances · 2026Review
- SMARCA4 Loss Promotes Late-Stage Tumor Progression in Nonneuroendocrine Small Cell Lung Cancer.Molecular cancer research : MCR · 2026Article
- Small Cell Lung Cancer Classification: Unraveling Heterogeneity to Enable Personalized Treatments.Cancer research · 2026Review
- mSWI/SNF complex inhibition sensitizes KRAS-mutant lung cancers to targeted therapies via epithelial-mesenchymal subversion.bioRxiv : the preprint server for biology · 2026Article
- Targeted regeneration of post-radiation epithelium without promoting cancer recurrence.Research square · 2026Article
- Chromatin remodeler BAF maintains HBV cccDNA transcriptional competence and represents a therapeutic target.Nucleic acids research · 2026Article
- Single-cell analysis identifies a VIM+ glioma stem-like vascular-immune state linked to myeloid OSM signaling and CEBPD activity.Frontiers in immunology · 2026Article
- Adjunctive diagnostic utility of POU2F3 in predominantly pulmonary high-grade neuroendocrine carcinomas with limited or discordant conventional marker expression: a case-control study.Frontiers in medicine · 2026Article
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Abstract
Small cell lung cancers (SCLCs) are composed of heterogeneous subtypes marked by lineage-specific transcription factors, including ASCL1, NEUROD1, and POU2F3. POU2F3-positive SCLCs, ∼12% of all cases, are uniquely dependent on POU2F3 itself; as such, approaches to attenuate POU2F3 expression may represent new therapeutic opportunities. Here using genome-scale screens for regulators of POU2F3 expression and SCLC proliferation, we define mSWI/SNF complexes as top dependencies specific to POU2F3-positive SCLC. Notably, chemical disruption of mSWI/SNF ATPase activity attenuates proliferation of all POU2F3-positive SCLCs, while disruption of non-canonical BAF (ncBAF) via BRD9 degradation is effective in pure non-neuroendocrine POU2F3-SCLCs. mSWI/SNF targets to and maintains accessibility over gene loci central to POU2F3-mediated gene regulatory networks. Finally, clinical-grade pharmacologic disruption of SMARCA4/2 ATPases and BRD9 decreases POU2F3-SCLC tumor growth and increases survival in vivo. These results demonstrate mSWI/SNF-mediated governance of the POU2F3 oncogenic program and suggest mSWI/SNF inhibition as a therapeutic strategy for POU2F3-positive SCLCs.
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