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Evaluation of calcium-binding protein A11 promotes the carcinogenesis of hypopharygeal squamous cell carcinoma via the PI3K/AKT signaling pathway

机译:钙结合蛋白A11的评估可通过PI3K / AKT信号通路促进下咽鳞状细胞癌的癌变

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摘要

Background: The S100 gene family encodes low molecular weight proteins implicated in cancer progression. In the present study, we explored the effects and underlying mechanisms of calcium-binding protein A11 (S100A11 protein) in hypopharyngeal squamous cell carcinoma (HSCC). Methods: RT-qPCR and western blot analysis were used to detect the mRNA and protein expression of S100A11, EGFR, MMP2, CD44, and MMP9. CCK-8, colony formation, wound healing and transwell invasion assays were performed to evaluate the effects of S100A11 on HSCC cells. Results: In our study, we observed that the level of S100A11 expression was significantly upregulated in HSCC tissues and cell lines. S100A11 inhibition increased the effects of 5-Fu on FaDu cells proliferation in vitro. In addition, S100A11 inhibition decreased the migration ability of FaDu cells. Additionally, the expression of migration-related proteins including EGFR, MMP2, CD44, and MMP9 were down-regulated when S100A11 was knocked down. Moreover, the expression of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR) and BCL-2 in FaDu cells were dramatically decreased. Conclusions: Our results suggested that S100A11 could activate the PI3K/Akt/mTOR signaling pathway in HSCC tumorigenesis.
机译:背景:S100基因家族编码与癌症发展有关的低分子量蛋白质。在本研究中,我们探讨了钙结合蛋白A11(S100A11蛋白)在下咽鳞状细胞癌(HSCC)中的作用及其潜在机制。方法:采用RT-qPCR和western blot方法检测S100A11,EGFR,MMP2,CD44和MMP9的mRNA和蛋白表达。进行CCK-8,集落形成,伤口愈合和transwell侵袭测定以评估S100A11对HSCC细胞的作用。结果:在我们的研究中,我们观察到HSCC组织和细胞系中S100A11表达水平显着上调。 S100A11抑制作用增强了5-Fu对FaDu细胞体外增殖的影响。此外,S100A11抑制降低了FaDu细胞的迁移能力。此外,当S100A11被敲低时,与迁移相关的蛋白(包括EGFR,MMP2,CD44和MMP9)的表达也被下调。而且,FaDu细胞中磷酸化PI3K(p-PI3K),磷酸化Akt(p-Akt),磷酸化mTOR(p-mTOR)和BCL-2的表达显着降低。结论:我们的结果表明,S100A11可以激活HSCC肿瘤发生过程中的PI3K / Akt / mTOR信号通路。

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