ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2014
Notch ligand Delta-like 1 promotes the metastasis of melanoma by enhancing tumor adhesion.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Double-sided niche regulation in skin stem cell and cancer: mechanisms and clinical applications.Molecular cancer · 2025Review
- Article
- miR-130b suppresses the invasion and migration of prostate cancer via inhibiting DLL1 and regulating the PI3K/Akt pathways.Experimental and therapeutic medicine · 2022Article
- Identification of Estrogen Signaling in a Prioritization Study of Intraocular Pressure-Associated Genes.International journal of molecular sciences · 2021Article
- BRN2 is a non-canonical melanoma tumor-suppressor.Nature communications · 2021Article
- Bone marrow mesenchymal stem cells promote prostate cancer cell stemness via cell-cell contact to activate the Jagged1/Notch1 pathway.Cell & bioscience · 2021Article
- The Role of DLLs in Cancer: A Novel Therapeutic Target.OncoTargets and therapy · 2020Review
- Article
- Article
- In Vitro Evaluation of Notch Inhibition to Enhance Efficacy of Radiation Therapy in Melanoma.Advances in radiation oncologyArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Notch signaling plays a vital role in tumorigenicity and tumor progression by regulating proliferation, invasion, and the tumor microenvironment. Previous research by our group indicated that Notch ligand Delta-like 1 (Dll1) is involved in angiogenesis in melanoma, and we noticed that it took a longer time to trypsinize Dll1-expressing B16 melanoma cells than the control cells. In this article, we extended our study to investigate the effects of Dll1 on tumor cell adhesion and metastasis. Dll1 overexpression activated Notch signaling in B16 tumor cells and significantly enhanced the adhering capacity of B16 tumor cells both in vitro and in vivo. B16-Dll1 cells also had a higher metastatic potential than their counterpart in the mouse model of lung metastasis. Along with increased Dll1 expression, N-cadherin, but not E-cadherin, was upregulated in B16-Dll1 cells. These data suggested that Notch ligand Dll1 may enhance the adhesion and metastasis of melanoma cells by upregulation of N-cadherin.
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Registered trials
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