ArticleThe Journal of clinical investigation2018
Notch-effector CSL promotes squamous cell carcinoma by repressing histone demethylase KDM6B.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- The Role of Chemopreventive Agents in the Management of Oral Potentially Malignant Disorders and Oral Cancer: A Narrative Review.Cancer reports (Hoboken, N.J.) · 2026Review
- Structural landscape of H3K27me3 recognition by protein domains and their potential for inhibition.The Journal of biological chemistry · 2026Review
- Epigenomic regulation of stemness contributes to the low immunogenicity of the most mutated human cancer.Cell reports · 2025Article
- T helper 2 cell-directed immunotherapy eliminates precancerous skin lesions.The Journal of clinical investigation · 2025Article
- Developments and future prospects of personalized medicine in head and neck squamous cell carcinoma diagnoses and treatments.Cancer reports (Hoboken, N.J.) · 2024Review
- Article
- ANKRD1 is a mesenchymal-specific driver of cancer-associated fibroblast activation bridging androgen receptor loss to AP-1 activation.Nature communications · 2024Article
- Identification of a Notch transcriptomic signature for breast cancer.Breast cancer research : BCR · 2024Article
- Comprehensive analysis of skin growth-related hub genes and microenvironment characterization in a mouse expanded skin model.Frontiers in immunology · 2024Article
- The ULK3 kinase is a determinant of keratinocyte self-renewal and tumorigenesis targeting the arginine methylome.Nature communications · 2023Article
- Evaluation of trabecular meshwork-specific promotersInternational journal of ophthalmology · 2023Article
- KDM6B promotes gastric carcinogenesis and metastasis via upregulation of CXCR4 expression.Cell death & disease · 2022Article
- Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022Review
- Review
- A Pan-Cancer Analysis Revealing the Dual Roles of Lysine (K)-Specific Demethylase 6B in Tumorigenesis and Immunity.Frontiers in genetics · 2022Article
- Colon cancer cells secreted CXCL11 via RBP-Jκ to facilitated tumour-associated macrophage-induced cancer metastasis.Journal of cellular and molecular medicine · 2021Article
- HSD17B7 gene in self-renewal and oncogenicity of keratinocytes from Black versus White populations.EMBO molecular medicine · 2021Article
- Notch-ing up knowledge on molecular mechanisms of skin fibrosis: focus on the multifaceted Notch signalling pathway.Journal of biomedical science · 2021Review
- KDM6B is an androgen regulated gene and plays oncogenic roles by demethylating H3K27me3 at cyclin D1 promoter in prostate cancer.Cell death & disease · 2021Article
- KDM6 Demethylases and Their Roles in Human Cancers.Frontiers in oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Notch 1/2 genes play tumor-suppressing functions in squamous cell carcinoma (SCC), a very common malignancy in skin and internal organs. In contrast with Notch, we show that the transcription factor CSL (also known as RBP-Jκ), a key effector of canonical Notch signaling endowed with intrinsic transcription-repressive functions, plays a tumor-promoting function in SCC development. Expression of this gene decreased in upper epidermal layers and human keratinocytes (HKCs) undergoing differentiation, while it increased in premalignant and malignant SCC lesions from skin, head/neck, and lung. Increased CSL levels enhanced the proliferative potential of HKCs and SCC cells, while silencing of CSL induced growth arrest and apoptosis. In vivo, SCC cells with increased CSL levels gave rise to rapidly expanding tumors, while cells with silenced CSL formed smaller and more differentiated tumors with enhanced inflammatory infiltrate. Global transcriptomic analysis of HKCs and SCC cells with silenced CSL revealed major modulation of apoptotic, cell-cycle, and proinflammatory genes. We also show that the histone demethylase KDM6B is a direct CSL-negative target, with inverse roles of CSL in HKC and SCC proliferative capacity, tumorigenesis, and tumor-associated inflammatory reaction. CSL/KDM6B protein expression could be used as a biomarker of SCC development and indicator of cancer treatment.
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Registered trials
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.