
VEGFR-1 can promote invasion through epithelial-mesenchymal transition induction in hepatocellular carcinoma (HCC). This study aims to elucidate VEGFR-1 impact on proteolytic enzymes profile involved with invasion.The effect on cell invasion was evaluated by invasive and migration assays with and without VEGFR-1 activation. The mechanism was investigated by real-time PCR, western blot and gelatin zymography using inhibitors for MMP-9. In total, 95 HCC patients were enrolled for its clinical value evaluation.VEGFR-1 activation induced invasion in HCC cells with an increase in the expression and activity of MMP-9 and Snail. MMP-9 blockage effectively inhibited VEGFR-1-induced invasion. High coexpression of both in HCC predicted a worse clinical outcome.Data show a novel VEGFR-1 activation-to-MMP-9 mechanism promoting HCC invasion.
Adult, Male, Carcinoma, Hepatocellular, Vascular Endothelial Growth Factor Receptor-1, Liver Neoplasms, Gene Expression, Middle Aged, Tumor Burden, Matrix Metalloproteinase 9, Cell Movement, Cell Line, Tumor, Humans, Female, Neoplasm Invasiveness, Snail Family Transcription Factors, Neoplasm Metastasis, Aged, Neoplasm Staging, Transcription Factors
Adult, Male, Carcinoma, Hepatocellular, Vascular Endothelial Growth Factor Receptor-1, Liver Neoplasms, Gene Expression, Middle Aged, Tumor Burden, Matrix Metalloproteinase 9, Cell Movement, Cell Line, Tumor, Humans, Female, Neoplasm Invasiveness, Snail Family Transcription Factors, Neoplasm Metastasis, Aged, Neoplasm Staging, Transcription Factors
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