ArticleMolecular cancer research : MCR2024
ORAOV1, CCND1, and MIR548K Are the Driver Oncogenes of the 11q13 Amplicon in Squamous Cell Carcinoma.
Article in Molecular cancer research : MCR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- Molecular and Immune Landscape of Recurrent and/or Distant Metastatic Squamous Cell Carcinoma of the Head and Neck: An EORTC/IMMUCAN Project.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Oncogene amplification of CCND1 via extrachromosomal DNA impacts overall survival in head and neck squamous cell carcinoma.Discover oncology · 2026Article
- Molecular and Cell Biological Characterization of Patient-Derived Head and Neck Squamous Carcinoma Cell Lines.Cancer science · 2026Article
- ZNF655 promotes tumor growth and chemoresistance by targeting MAFF-CCND1 axis in ovarian cancer.Cancer cell international · 2025Article
- Tumor-infiltrating nociceptor neurons promote immunosuppression.Science signaling · 2025Article
- Screening of Hub Genes and Therapeutic Drugs in Cervical Cancer Using Integrated Bioinformatics Analysis.Journal of Cancer · 2025Article
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6 authors at 2 institutions in 1 country.
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Abstract
11q13 amplification is a frequent event in human cancer and in particular in squamous cell carcinomas (SCC). Despite almost invariably spanning 10 genes, it is unclear which genetic components of the amplicon are the key driver events in SCC. A combination of computational, in vitro, ex vivo, and in vivo models leveraging efficient primary human keratinocyte genome editing by Cas9-RNP electroporation, identified ORAOV1, CCND1, and MIR548K as the critical drivers of the amplicon in head and neck SCC. CCND1 amplification drives the cell cycle in a CDK4/6/RB1-independent fashion and may confer a novel dependency on RRM2. MIR548K contributes to epithelial-mesenchymal transition. Finally, we identify ORAOV1 as an oncogene that acts likely via its ability to modulate reactive oxygen species. Thus, the 11q13 amplicon drives SCC through at least three independent genetic elements and suggests therapeutic targets for this morbid and lethal disease. IMPLICATIONS: This work demonstrates novel mechanisms and ways to target these mechanisms underlying the most common amplification in squamous cell carcinoma, one of the most prevalent and deadly forms of human cancer.
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