Fisetin inhibits vascular endothelial growth factor‑induced angiogenesis in retinoblastoma cells
- Liangjun Wang
- Ning Chen
- Hongxia Cheng
Affiliations: Department of Ophthalmology, Yantai Mountain Hospital, Yantai, Shandong 264001, P.R. China, Department of Ophthalmology, Yuhuangding Hospital, Yantai, Shandong 264000, P.R. China
- Published online on: May 28, 2020 https://doi.org/10.3892/ol.2020.11679
Copyright: © Wang
et al. This is an open access article distributed under the
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Fisetin is a small phytochemical molecule with antitumor activity. Angiogenesis is a basic process that occurs during tumor growth and metastasis. The vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) pathway is a key regulator of angiogenesis. The aim of the present study was to evaluate whether fisetin affects angiogenesis through the VEGFR pathway. In the present study, Y79 cells were treated with 100 ng/ml VEGF in the presence of fisetin at concentrations of 0, 25, 50 and 100 µM. A Cell Counting Kit‑8 assay was used to detect proliferation and the Transwell and Matrigel assays were used to assess cell migration and invasion, respectively. Reverse transcription‑quantitative polymerase chain reaction analysis was applied to measure the expression level of VEGFR mRNA and western blot analysis was used to measure the protein expression of VEGFR. An immunofluorescence assay was used to detect the expression of VEGFR. Angiogenesis in vitro was assessed by a tube formation assay. The results demonstrated that fisetin significantly inhibited the proliferation of Y79 cells in a time‑ and dose‑dependent manner. Fisetin also inhibited the migration and invasion of Y79 cells in a dose‑dependent manner. Furthermore, fisetin inhibited the expression of VEGFR in Y79 cells in a dose‑dependent manner and tumor angiogenesis in vitro. Thus, fisetin was found to inhibit angiogenesis via inhibition of the VEGF/VEGFR signaling pathway, and could be used as a candidate drug to inhibit angiogenesis in retinoblastoma.