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The interaction of HAb18G/CD147 with integrin α6β1 and its implications for the invasion potential of human hepatoma cells

机译:HAb18G / CD147与整合素α6β1的相互作用及其对人肝癌细胞侵袭潜能的影响

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Background HAb18G/CD147 plays pivotal roles in invasion by hepatoma cells, but the underlying mechanism remains unclear. Our previous study demonstrated that overexpression of HAb18G/CD147 promotes invasion by interacting with integrin α3β1. However, it has never been investigated whether α3β1 is solely responsible for this process or if other integrin family members also interact with HAb18G/CD147 in human hepatoma cells. Methods Human SMMC-7721 and FHCC98 cells were cultured and transfected with siRNA fragments against HAb18G/CD147. The expression levels of HAb18G/CD147 and integrin α6β1 were determined by immunofluorescent double-staining and confocal imaging analysis. Co-immunoprecipitation and Western blot analyses were performed to examine the native conformations of HAb18G/CD147 and integrin α6β1. Invasion potential was evaluated with an invasion assay and gelatin zymography. Results We found that integrin α6β1 co-localizes and interacts with HAb18G/CD147 in human hepatoma cells. The enhancing effects of HAb18G/CD147 on invasion capacity and secretion of matrix metalloproteinases (MMPs) were partially blocked by integrin α6β1 antibodies ( P 2+ mobilization, significantly reduced cell invasion potential and secretion of MMPs in human hepatoma cells ( P Conclusion These results suggest that α6β1 interacts with HAb18G/CD147 to mediate tumor invasion and metastatic processes through the PI3K pathway.
机译:背景HAb18G / CD147在肝癌细胞侵袭中起关键作用,但其潜在机制尚不清楚。我们先前的研究表明,HAb18G / CD147的过表达通过与整联蛋白α3β1相互作用来促进侵袭。但是,从未研究过α3β1是否仅负责此过程,或者其他整联蛋白家族成员是否也与人肝癌细胞中的HAb18G / CD147相互作用。方法培养人SMMC-7721和FHCC98细胞,并用针对HAb18G / CD147的siRNA片段转染。通过免疫荧光双染色和共聚焦成像分析确定HAb18G / CD147和整联蛋白α6β1的表达水平。进行了免疫共沉淀和蛋白质印迹分析,以检查HAb18G / CD147和整联蛋白α6β1的天然构象。用侵袭测定法和明胶酶谱法评估侵袭潜能。结果我们发现整联蛋白α6β1在人肝癌细胞中共定位并与HAb18G / CD147相互作用。 HAb18G / CD147对整合素α6β1抗体的侵袭能力和基质金属蛋白酶(MMPs)分泌的增强作用(P 2 + 动员,显着降低了人肝癌细胞的侵袭能力和MMPs的分泌(P结论这些结果表明,α6β1与HAb18G / CD147相互作用,通过PI3K途径介导肿瘤侵袭和转移过程。

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