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Establishment of an oral squamous cell carcinoma cell line expressing vascular endothelial growth factor a and its two receptors

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 progno...

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Detalles Bibliográficos
Autores principales: Araki-Maeda, Hanako, Kawabe, Mutsuki, Omori, Yuji, Yamanegi, Koji, Yoshida, Kazunari, Yoshikawa, Kyohei, Takaoka, Kazuki, Noguchi, Kazuma, Nakano, Yoshiro, Kishimoto, Hiromitsu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Association for Dental Sciences of the Republic of China 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9588810/
https://www.ncbi.nlm.nih.gov/pubmed/36299342
http://dx.doi.org/10.1016/j.jds.2022.04.018
Descripción
Sumario: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.