ArticleJournal of dental sciences2022
Establishment of an oral squamous cell carcinoma cell line expressing vascular endothelial growth factor a and its two receptors.
Article in Journal of dental sciences, 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.
- Cinobufagin inhibits hepatocellular carcinoma EMT-like stemness via VEGF/VEGFR2 autocrine signaling.Discover oncology · 2025Article
- Erianin inhibits cell migration and induces apoptosis by inhibiting VEGF-α/PI3K/AKT signaling pathway in malignant melanoma.Scientific reports · 2025Article
- Mechanism of Tumor Budding in Patient-Derived Metachronous Oral Primary Squamous Cell Carcinoma Cell Lines.International journal of molecular sciences · 2025Article
- S-palmitoylation: a novel insight in the development and immunotherapy of oral squamous cell carcinoma.Journal of Cancer · 2025Review
- Salivary miRNAs as a novel therapeutic marker in a patient with advanced oral squamous cell carcinoma: A case report.Oncology letters · 2025Article
- Bacterial Lipopolysaccharide Induces PD-L1 Expression and an Invasive Phenotype of Oral Squamous Cell Carcinoma Cells.Cancers · 2024Article
- GC-MS analysis, pharmacokinetic properties, molecular docking and dynamics simulation of bioactives fromIn silico pharmacology · 2024Article
- Inhibition of VEGFR2 and EGFR signaling cooperatively suppresses the proliferation of oral squamous cell carcinoma.Cancer medicine · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Vascular endothelial growth factor receptor (VEGFR) expression in oral squamous cell carcinoma (OSCC) promotes tumor growth through both autocrine and paracrine signaling. VEGF-positive OSCC cases are associated with a high depth of invasion, increased metastasis, and poor prognosis. In this study we established and then molecularly and functionally analyzed an OSCC cell line that co-expresses VEGF-A, VEGFR-1, and VEGFR-2, termed HCM-SqCC010 cells. Materials and methods: VEGF-A, VEGFR-1, and VEGFR-2 expression in HCM-SqCC010 cells were examined by immunohistochemistry and immunoblotting. Expression and inhibition of VEGF-A, VEGFR-1, and VEGFR-2 in HCM-SqCC010 cells were verified by quantitative real-time PCR. Results: Our analysis of HCM-SqCC010 cells revealed that their proliferation depended on VEGF-A, and selective inhibition of VEGFR-1 or VEGFR-2 resulted in decreased cell growth. Conclusion: We established an OSCC cell line, HCM-SqCC010, that expresses VEGF-A, VEGFR-1, and VEGFR-2. This triple-positive cell line showed no effect from a molecular targeted drug toward VEGF-A, but it did show strong cell growth inhibition in response to a VEGFR inhibitor. Thus, new therapeutic strategies against OSCC should include a VEGFR inhibitor.
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