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Objective: Very low density lipoprotein receptor (VLDLR) has been considered as a multiple function receptor due to binding numerous ligands, causing endocytosis and regulating cellular signaling. Our group previously reported that type Ⅱ VLDLR overexpression in breast cancer tissues. The purpose of this study is to characterize type Ⅱ VLDLR activities during cell migration using breast cancer cell lines. Methods: Western blotting was used to test protein expression. Cell migration was analyzed by Scratch wound assay. The mRNA expression was tested by realtime-PCR. Reporter assay was to test the transcription activity. Results: Scratch wound and Report assay indicated up-regulated VLDLR Ⅱ expression promotes cell migration via activating Wnt/β-catenin pathway. The target genes such as VEGF, MMP2 and MMP7 were upregulated in VLDLR Ⅱ overexpressed cells. On the contrary, cells treated with TFPI had an inhibition effect of cell migration response to down-regulation of VLDLR Ⅱ. Conclusion: Type Ⅱ VLDLR conferred a migration and invasion advantage by activating Wnt/β-catenin pathway, then up-regulating VEGF, MMP2 and MMP7 in breast cancer cells.
Objective: Very low density lipoprotein receptor (VLDLR) has been considered as a multiple function receptor due to binding multiple ligands, causing causing endocytosis and regulating cellular signaling. Our group previously reported that type II VLDLR overexpression in breast cancer tissues. The purpose of this study is to characterize type II VLDLR activities during cell migration using breast cancer cell lines. Methods: Western blotting was used to test protein expression. Cell migration was analyzed by Scratch wound assay. The mRNA expression was tested by realtime-PCR. Reporter assay was to Test the transcription activity. Results: Scratch wound and Report assay indicated up-regulated VLDLRII expression promotes cell migration via activating Wnt / beta-catenin pathway. The target genes such as VEGF, MMP2 and MMP7 were upregulated in VLDLR overexpressed cells. On the contrary, cells treated with TFPI had an inhibition effect of cell migration response to down-regulation of VLDLR II. Conclusion: Type II VLDLR conferred a migration and invasion advantage by activating Wnt / β-catenin pathway, then up-regulating VEGF, MMP2 and MMP7 in breast cancer cells.