ArticleCellular oncology (Dordrecht, Netherlands)2022
Inhibition of CD146 lessens uveal melanoma progression through reducing angiogenesis and vasculogenic mimicry.
Article in Cellular oncology (Dordrecht, Netherlands), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Knockout of PAK1 and PAK4 supresses tumour growth associated with vasculogenic mimicry inhibition through EphA2-VE-cadherin-MCAM pathway.Cell communication and signaling : CCS · 2026Article
- CD146Theranostics · 2026Article
- The multifaceted roles of MCAM in development, homeostasis, pathological conditions, and cancer.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Unraveling vascular mechanisms in melanoma: roles of angiogenesis and vasculogenic mimicry in tumor progression and therapeutic resistance.Cancer biology & medicine · 2025Review
- MUC18-Directed chimeric antigen receptor T cells for the treatment of mucosal melanoma.Journal of translational medicine · 2025Article
- CD146 regulates the stemness and chemoresistance of hepatocellular carcinoma via JAG2-NOTCH signaling.Cell death & disease · 2025Article
- PLEK2: a potential biomarker for metastasis and prognostic evaluation in uveal melanoma.Frontiers in medicine · 2024Article
- CD146 promotes resistance of NSCLC brain metastases to pemetrexed via the NF-κB signaling pathway.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAnti-angiogenesis drug therapy is ineffective in treating uveal melanoma since it only targets angiogenesis leaving vasculogenic mimicry aside. There is no effective clinical strategy targeting vasculogenic mimicry, yet. We show here that CD146 is a novel target to inhibit uveal melanoma progression since it regulates both uveal melanoma angiogenesis and vasculogenic mimicry activity.
methodsCD146 inhibition was achieved with its specific siRNAs or antibody AA98. Tube formation and migration of primary human retinal microvascular endothelial cells and tube-like structure formation, migration, invasion of uveal melanoma cells were evaluated after CD146 inhibition. The underlying mechanisms were investigated by Western blot and immunofluorescence. Finally, uveal melanoma cells were injected subretinally into the eyes of nude mice and AA98 was administrated. Tumor size was revealed by H&E staining, and angiogenesis and vasculogenic mimicry were evaluated with CD31-PAS staining.
resultsCD146 inhibition induced declines in tube formation and migration of primary human retinal microvascular endothelial cells and tube-like structure formation of uveal melanoma cells. CD146 mediated VEGFR/AKT/p38/NF-κB and FAK/VE-cadherin signal cascades were partially responsible for these biological effects. CD146 blockade by siRNA or AA98 also resulted in inhibition of migration and invasion as well as EMT process of uveal melanoma cells. The physiological relevance of such declines was confirmed by showing that AA98 treatment markedly suppressed the tumor growth, angiogenesis and vasculogenic mimicry induced by implantation of uveal melanoma cells into the eyes of nude mice.
conclusionsCD146 is a novel mediator of both angiogenesis and vasculogenic mimicry in uveal melanoma. Its antibody AA98 has the potency to be developed as a new antibody drug for treating uveal melanoma. Our results warrant further assessment of CD146 as a potential target to improve therapeutic management of uveal melanoma in a clinical setting.
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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 Socratic graph.