ArticleCell proliferation2019
Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial-mesenchymal transition in salivary adenoid cystic carcinoma.
Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.
- Pooled it
- WISP2 Overexpression Is Associated with Reduced Vasculogenic Mimicry and Epithelial-Mesenchymal Transition in Gastric Cancer.Digestive diseases and sciences · 2026Article
- Evaluation of Serum HIF-1α as a Hypoxia-Related Biomarker in Patients with Malignant Salivary Gland Neoplasms.Biomedicines · 2026Article
- Rewiring cancer cell fate toward vasculogenic mimicry: from classical to unconventional processes.Cancer metastasis reviews · 2026Review
- Vascular Endothelial Barrier in Salivary Glands: From Physiological Regulation to Pathological Impairment of Secretion.International journal of molecular sciences · 2026Review
- CD147-positive migrasome macropinocytosis promotes HCC sorafenib resistance via inducing vasculogenic mimicry triggered by PI3K/AKT/TWIST1 signaling.Cell death & disease · 2026Article
- Tissue Homogenate VEGF Levels in Malignant Salivary Gland Tumors vs. Controls: An Exploratory Pilot Study.Journal of clinical medicine · 2026Article
- Acidosis Drives Vasculogenic Mimicry in PDAC CSCs via Na+/H+ Exchanger Isoform 1 (NHE1) and Calcium Entry.Cells · 2026Article
- Correction: Myeloid derived suppressor cells contribute to the malignant progression of oral squamous cell carcinoma.PloS one · 2026Article
- VaMiAnalyzer: an open source, Python-based application for analysis of 3D in vitro vasculogenic mimicry assays.BMC bioinformatics · 2025Article
- Cancer-associated fibroblasts expressing FSTL3 promote vasculogenic mimicry formation and drive colon cancer malignancy.Cell death & disease · 2025Article
- Review
- Review
- Cetuximab and Paclitaxel Drug Response in Head and Neck Tumor Stem Cells.Biomolecules · 2025Article
- A novel vasculogenic mimicry-related nomogram predicts prognosis in hepatocellular carcinoma.Frontiers in genetics · 2025Article
- A review of the roles of exosomes in salivary gland diseases with an emphasis on primary Sjögren's syndrome.Journal of dental sciences · 2025Review
- JAM3 promotes cervical cancer metastasis by activating the HIF-1α/VEGFA pathway.BMC women's health · 2024Article
- ESM1 enhances fatty acid synthesis and vascular mimicry in ovarian cancer by utilizing the PKM2-dependent warburg effect within the hypoxic tumor microenvironment.Molecular cancer · 2024Article
- RUNX1-BMP2 promotes vasculogenic mimicry in laryngeal squamous cell carcinoma via activation of the PI3K-AKT signaling pathway.Cell communication and signaling : CCS · 2024Article
- Pan-cancer dissection of vasculogenic mimicry characteristic to provide potential therapeutic targets.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesTo investigate the role of hypoxia in vasculogenic mimicry (VM) of salivary adenoid cystic carcinoma (SACC) and the underlying mechanism involved. MATERIALS AND
methodsFirstly, wound healing, transwell invasion, immunofluorescence and tube formation assays were performed to measure the effect of hypoxia on migration, invasion, EMT and VM of SACC cells, respectively. Then, immunofluorescence and RT-PCR were used to detect the effect of hypoxia on VE-cadherin and VEGFA expression. And pro-vasculogenic mimicry effect of VEGFA was investigated by confocal laser scanning microscopy and Western blot. Moreover, the levels of E-cadherin, N-cadherin, Vimentin, CD44 and ALDH1 were determined by Western blot and immunofluorescence in SACC cells treated by exogenous VEGFA or bevacizumab. Finally, CD31/ PAS staining was performed to observe VM and immunohistochemistry was used to determine the levels of VEGFA and HIF-1α in 95 SACC patients. The relationships between VM and clinicopathological variables, VEGFA or HIF-1α level were analysed.
resultsHypoxia promoted cell migration, invasion, EMT and VM formation, and enhanced VE-cadherin and VEGFA expression in SACC cells. Further, exogenous VEGFA markedly increased the levels of N-cadherin, Vimentin, CD44 and ALDH1, and inhibited the expression of E-cadherin, while the VEGFA inhibitor reversed these changes. In addition, VM channels existed in 25 of 95 SACC samples, and there was a strong positive correlation between VM and clinic stage, distant metastases, VEGFA and HIF-1α expression.
conclusionsVEGFA played an important role in hypoxia-induced VM through regulating EMT and stemness, which may eventually fuel the migration and invasion of SACC.
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