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首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >Inhibition of EGF-induced migration and invasion by sulfated polysaccharide of Sepiella maindroni ink via the suppression of EGFR/Akt/p38 MAPK/MMP-2 signaling pathway in KB cells
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Inhibition of EGF-induced migration and invasion by sulfated polysaccharide of Sepiella maindroni ink via the suppression of EGFR/Akt/p38 MAPK/MMP-2 signaling pathway in KB cells

机译:通过在KB细胞中抑制EGFR / AKT / P38 Mapk / MMP-2信号通路的抑制EGF诱导的EGF诱导的血液多糖的迁移和侵袭

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Highlights ? Sulfated polysaccharide of Sepiella maindroni ink (SIP-SII) inhibited EGF-induced migration and invasion in KB cells. ? SIP-SII inhibited the EGF-induced MMP-2 expression markedly in KB cells. ? SIP-SII attenuated the EGF-induced migration and invasion of KB cells via suppressing the EGFR/Akt/p38 MAPK/MMP-2 pathway. Abstract SIP-SII, the sulfated Sepiella maindroni ink polysaccharide (SIP), has been manifested to possess anti-tumor and anti-metastasis activity in vivo and in vitro . In the present study, we evaluated its inhibitory effect on the epidermal growth factor (EGF)-induced migration and invasion of human epidermoid carcinoma cell (KB cell line) as well as the related signaling pathways. The results of MTT assay indicated that SIP-SII inhibited the proliferation of KB cells in a concentration and time dependent manner. Notably, the attenuation of cell growth by SIP-SII was enlarged in the presence of EGF. The wound healing assay and transwell invasion assay were used to evaluate the effect of SIP-SII on the EGF-induced migration and invasion of KB cells and the results showed that SIP-SII markedly attenuated the EGF-induced migration and invasion. Besides, the EGF-induced matrix metalloproteinase-2 (MMP-2) expression was also suppressed by SIP-SII. However, SIP-SII showed no significant inhibition of the EGF-induced matrix metalloproteinase-9 (MMP-9) expression. Further research revealed that SIP-SII decreased the EGF-induced phosphorylation of epidermal growth factor receptor (EGFR), Akt and p38, but no significant suppression on EGF-induced phosphorylation of extracellular signal-regulated kinase 1 and 2 (Erk1/2) and c-Jun N-terminal kinases (JNK) by SIP-SII treatment was observed. The involvement of EGFR/Akt/p38 pathway was confirmed by evidence that SIP-SII would enlarge the inhibitory effect of the specific signal pathway inhibitors. These results indicate that SIP-SII has the potential to be used as the inhibitor of tumor metastasis especially for cancers characterized by over-activation of EGF/EGFR signaling. ]]>
机译:强调 ? Sepiella maindroni油墨(SiP-Sii)的硫酸化多糖抑制了KB细胞中的EGF诱导的迁移和侵袭。还SIP-SII在KB细胞中抑制EGF诱导的MMP-2表达。还SIP-SII通过抑制EGFR / AKT / P38 MAPK / MMP-2途径,衰减EGF诱导的KB细胞迁移和侵袭。摘要SIP-SII,硫酸盐SEPIELLA MAINDRONI墨水多糖(SIP),已经表现为体内和体外具有抗肿瘤和抗转移活性。在本研究中,我们评估其对表皮生长因子(EGF)的抑制作用 - 诱导人表皮癌细胞(KB细胞系)以及相关信号通路的迁移和侵袭。 MTT测定的结果表明,SIP-SII以浓度和时间依赖性方式抑制KB细胞的增殖。值得注意的是,在EGF存在下,SIP-SII对细胞生长的衰减扩大。伤口愈合测定和Transwell侵袭测定用于评估SIP-SII对KB细胞EGF诱导的迁移和侵袭的影响,结果表明,SIP-SII显着减弱了EGF诱导的迁移和侵袭。此外,SIP-SII还抑制了EGF诱导的基质金属蛋白酶-2(MMP-2)表达。然而,SIP-SII显示出对EGF诱导的基质金属蛋白酶-9(MMP-9)表达的显着抑制。进一步的研究表明,SIP-SII降低了表皮生长因子受体(EGFR),AKT和P38的EGF诱导的磷酸化,但对EGF诱导的细胞外信号调节激酶1和2(ERK1 / 2)的磷酸化没有显着抑制通过SIP-SII治疗观察C-Jun N-末端激酶(JNK)。通过证据证明EGFR / AKT / P38途径的涉及SIP-SII将扩大特定信号途径抑制剂的抑制作用。这些结果表明SIP-SII具有用作肿瘤转移的抑制剂,特别是对于以EGF / EGFR信号传导的过度激活而表征的癌症。 ]]>

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