ArticleOncogene2022
Therapeutic targeting of BAP1/ASXL3 sub-complex in ASCL1-dependent small cell lung cancer.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Tumor suppressor BAP1 emerges as a key regulator of metabolism and cell death in tumors.Frontiers in cell and developmental biology · 2026Review
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- UFMylation maintains tumor suppressor pVHL stability by activating the deubiquitinase BAP1.Science advances · 2025Article
- LN-439A, a novel BAP1 inhibitor, suppresses the growth of basal-like breast cancer by degrading KLF5.Acta pharmacologica Sinica · 2025Article
- An epigenetic pathway regulates MHC-II expression and function in B cell lymphoma models.The Journal of clinical investigation · 2025Article
- Enantioselective OTUD7B fragment discovery through chemoproteomics screening and high-throughput optimisation.Communications chemistry · 2025Article
- Case Report: A familial hematological pedigree reveals VHL germline mutation as a principal predisposition factor with additional mutations modulating phenotypic heterogeneity.Frontiers in oncology · 2025Article
- Integrative analysis of ASXL family genes reveals ASXL2 as an immunoregulatory molecule in head and neck squamous cell carcinoma.Scientific reports · 2024Article
- Therapeutic Exploitation of Neuroendocrine Transdifferentiation Drivers in Prostate Cancer.Cells · 2024Review
- Understanding the intersection between placental development and cancer: Lessons from the tumor suppressor BAP1.Communications biology · 2024Review
- Sex-specific survival gene mutations are discovered as clinical predictors of clear cell renal cell carcinoma.Scientific reports · 2024Article
- H2A monoubiquitination: insights from human genetics and animal models.Human genetics · 2024Review
- Lineage-specific intolerance to oncogenic drivers restricts histological transformation.Science (New York, N.Y.) · 2024Article
- Small Cell Lung Cancer Plasticity Enables NFIB-Independent Metastasis.Cancer research · 2024Article
- Potential roles of UCH family deubiquitinases in tumorigenesis and chemical inhibitors developed against them.American journal of cancer research · 2024Review
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- Deficiency of BAP1 inhibits neuroblastoma tumorigenesis through destabilization of MYCN.Cell death & disease · 2023Article
- A reappraisal of ASXL1 mutation sites and the cohesin-binding motif in myeloid disease.Blood cancer journal · 2023Article
- BAP1 in cancer: epigenetic stability and genome integrity.Discover oncology · 2022Review
- MBD5 and MBD6 stabilize the BAP1 complex and promote BAP1-dependent cancer.Genome biology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small cell lung cancer (SCLC) is an aggressive disease, with patients diagnosed with either early-stage, limited stage, or extensive stage of SCLC tumor progression. Discovering and targeting the functional biomarkers for SCLC will be crucial in understanding the molecular basis underlying SCLC tumorigenesis to better assist in improving clinical treatment. Emerging studies have demonstrated that dysregulations in BAP1 histone H2A deubiquitinase complex are collectively associated with pathogenesis in human SCLC. Here, we investigated the function of the oncogenic BAP1/ASXL3/BRD4 epigenetic axis in SCLC by developing a next-generation BAP1 inhibitor, iBAP-II, and focusing on the epigenetic balance established between BAP1 and non-canonical PRC1 complexes in regulating SCLC-specific transcriptional programming. We further demonstrated that pharmacologic inhibition of BAP1's catalytic activity disrupted BAP1/ASXL3/BRD4 epigenetic axis by inducing protein degradation of the ASXL3 scaffold protein, which bridges BRD4 and BAP1 at active enhancers. Furthermore, treatment of iBAP-II represses neuroendocrine lineage-specific ASCL1/MYCL/E2F signaling in SCLC cell lines, and dramatically inhibits SCLC cell viability and tumor growth in vivo. In summary, this study has provided mechanistic insight into the oncogenic function of BAP1 in SCLC and highlighted the potential of targeting BAP1's activity as a novel SCLC therapy.
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