ArticleThe Journal of pathology2013
The matricellular protein CCN3 regulates NOTCH1 signalling in chronic myeloid leukaemia.
Article in The Journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Effects of topological domain disruption on transcriptional regulation are chromatin context dependent.Epigenetics & chromatin · 2026Article
- Danlian-Tongmai formula improves diabetic vascular calcification by regulating CCN3/NOTCH signal axis to inhibit inflammatory reaction.Frontiers in pharmacology · 2024Article
- Single-cell RNA sequencing of solid pseudopapillary neoplasms of the pancreas in children.Cancer science · 2023Article
- Hes1 Controls Proliferation and Apoptosis in Chronic Lymphoblastic Leukemia Cells by Modulating PTEN Expression.Molecular biotechnology · 2022Article
- Histone chaperone ASF1A accelerates chronic myeloid leukemia blast crisis by activating Notch signaling.Cell death & disease · 2022Article
- The bioengineered HALOA complex induces anoikis in chronic myeloid leukemia cells by targeting the BCR-ABL/Notch/Ikaros/Redox/Inflammation axis.Journal of medicine and life · 2022Article
- CCN2 (Cellular Communication Network factor 2) in the bone marrow microenvironment, normal and malignant hematopoiesis.Journal of cell communication and signaling · 2021Review
- The Emerging Roles of CCN3 Protein in Immune-Related Diseases.Mediators of inflammation · 2021Review
- CCN3 (NOV) Drives Degradative Changes in Aging Articular Cartilage.International journal of molecular sciences · 2020Article
- Proteomics pinpoints alterations in grade I meningiomas of male versus female patients.Scientific reports · 2020Article
- Time-series analysis in imatinib-resistant chronic myeloid leukemia K562-cells under different drug treatments.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017Article
- CCN family of proteins: critical modulators of the tumor cell microenvironment.Journal of cell communication and signaling · 2016Article
- The role of the CCN family of proteins in blood cancers.Journal of cell communication and signaling · 2016Article
- The role of CCN family genes in haematological malignancies.Journal of cell communication and signaling · 2015Article
- The NOTCH signaling pathway in normal and malignant blood cell production.Journal of cell communication and signaling · 2015Article
- Potential role of Notch signalling in CD34+ chronic myeloid leukaemia cells: cross-talk between Notch and BCR-ABL.PloS one · 2015Article
- The challenge of targeting notch in hematologic malignancies.Frontiers in pediatrics · 2014Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulated NOTCH1 has been reported in lymphoid leukaemia, although its role in chronic myeloid leukaemia (CML) is not well established. We previously reported BCR-ABL down-regulation of a novel haematopoietic regulator, CCN3, in CML; CCN3 is a non-canonical NOTCH1 ligand. This study characterizes the NOTCH1–CCN3 signalling axis in CML. In K562 cells, BCR-ABL silencing reduced full-length NOTCH1 (NOTCH1-FL) and inhibited the cleavage of NOTCH1 intracellular domain (NOTCH1-ICD), resulting in decreased expression of the NOTCH1 targets c-MYC and HES1. K562 cells stably overexpressing CCN3 (K562/CCN3) or treated with recombinant CCN3(rCCN3) showed a significant reduction in NOTCH1 signalling (> 50% reduction in NOTCH1-ICD, p < 0.05).Gamma secretase inhibitor (GSI), which blocks NOTCH1 signalling, reduced K562/CCN3 colony formation but increased that of K562/control cells. GSI combined with either rCCN3 or imatinib reduced K562 colony formation with enhanced reduction of NOTCH1 signalling observed with combination treatments. We demonstrate an oncogenic role for NOTCH1 in CML and suggest that BCR-ABL disruption of NOTCH1–CCN3 signalling contributes to the pathogenesis of CML.
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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 Socratic graph.