ArticleThe Journal of clinical investigation2018
JAM3 maintains leukemia-initiating cell self-renewal through LRP5/AKT/β-catenin/CCND1 signaling.
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 39 papers.
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Who cites it
39 citing papers in PubMed, 83 citations in OpenAlex.
- Genetic deletion of JAM-C in preleukemic cells rewires leukemic stem cell gene expression program in AML.Blood advances · 2024Trial
- PAX1/JAM3 methylation-a novel biomarker for early detection and accurate management of cervical adenocarcinoma.American journal of cancer research · 2026Review
- Nonionotropic action of an acid-sensing ion channel inhibits leukemogenesis in the acidic bone marrow niche.The Journal of clinical investigation · 2025Article
- UCHL3 depletion inhibits gastric cancer progression and enhances palbociclib sensitivity by regulating the AKT/CCND1 signaling axis via ENO1 ubiquitination.Cell death & disease · 2025Article
- Review
- Junctional adhesion molecule-C: A multifunctional mediator of cell adhesion.Cellular and molecular life sciences : CMLS · 2025Review
- Epigenetic silencing of JAM3 promoted progression in serous ovarian carcinoma through PI3K/AKT pathway.Epigenomics · 2025Article
- A novel polypeptide encoded by circSPIRE1 promotes prostate cancer proliferation and migration by restraining the ubiquitin-dependent degradation of LRP5.Journal of experimental & clinical cancer research : CR · 2025Article
- Gut dysbiosis conveys psychological stress to activate LRP5/β-catenin pathway promoting cancer stemness.Signal transduction and targeted therapy · 2025Article
- MCM8 promotes NR4A1-mediated E2F1 transcription and facilitates renal cell carcinoma through enhancing aerobic glycolysis.Cell biology and toxicology · 2025Article
- CPSF6-RARγ interacts with histone deacetylase 3 to promote myeloid transformation in RARG-fusion acute myeloid leukemia.Nature communications · 2025Article
- Targeting ferroptosis: a promising avenue for ovarian cancer treatment.Frontiers in immunology · 2025Review
- Junctional adhesion molecular 3 (JAM3) is a novel tumor suppressor and improves the prognosis in breast cancer brain metastases via the TGF-β/Smad signal pathway.Journal of neuro-oncology · 2024Article
- DNAJC10 maintains survival and self-renewal of leukemia stem cells through PERK branch of the unfolded protein response.Haematologica · 2024Article
- JAM3: A prognostic biomarker for bladder cancer via epithelial-mesenchymal transition regulation.Biomolecules & biomedicine · 2024Article
- Downregulation of JAM3 occurs in cholangiocarcinoma by hypermethylation: A potential molecular marker for diagnosis and prognosis.Journal of cellular and molecular medicine · 2024Article
- Targeting cytohesin-1 suppresses acute myeloid leukemia progression and overcomes resistance to ABT-199.Acta pharmacologica Sinica · 2024Article
- Article
- Immunotherapy in leukaemia.Acta biochimica et biophysica Sinica · 2023Review
- Sox13 and M2-like leukemia-associated macrophages contribute to endogenous IL-34 caused accelerated progression of acute myeloid leukemia.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Leukemia-initiating cells (LICs) are responsible for the initiation, development, and relapse of leukemia. The identification of novel therapeutic LIC targets is critical to curing leukemia. In this report, we reveal that junctional adhesion molecule 3 (JAM3) is highly enriched in both mouse and human LICs. Leukemogenesis is almost completely abrogated upon Jam3 deletion during serial transplantations in an MLL-AF9-induced murine acute myeloid leukemia model. In contrast, Jam3 deletion does not affect the functions of mouse hematopoietic stem cells. Moreover, knockdown of JAM3 leads to a dramatic decrease in the proliferation of both human leukemia cell lines and primary LICs. JAM3 directly associates with LRP5 to activate the downstream PDK1/AKT pathway, followed by the downregulation of GSK3β and activation of β-catenin/CCND1 signaling, to maintain the self-renewal ability and cell cycle entry of LICs. Thus, JAM3 may serve as a functional LIC marker and play an important role in the maintenance of LIC stemness through unexpected LRP5/PDK1/AKT/GSK3β/β-catenin/CCND1 signaling pathways but not via its canonical role in cell junctions and migration. JAM3 may be an ideal therapeutic target for the eradication of LICs without influencing normal hematopoiesis.
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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.