Sulfated polysaccharide of Sepiella Maindroni ink inhibits the migration, invasion and matrix metalloproteinase-2 expression through suppressing EGFR-mediated p38/MAPK and PI3K/Akt/mTOR signaling pathways in SKOV-3 cells
文献类型： 外文期刊
作者： Jiang, Wenjie 1 ; Cheng, Yanna 2 ; Zhao, Na 1 ; Li, Lian 3 ; Shi, Yikang 4 ; Zong, Aizhen 5 ; Wang, Fengshan 1 ;
作者机构： 1.Shandong Univ, Inst Biochem & Biotechnol Drugs, Sch Pharmaceut Sci, Key Lab Chem Biol,Minist Educ, Jinan 250012, Shandong, Peoples R China
2.Shandong Univ, Sch Pharmaceut Sci, Dept Pharmacol, Jinan 250012, Shandong, Peoples R China
3.Shandong Univ, Sch Basic Med Sci, Jinan 250012, Shandong, Peoples R China
4.Shandong Univ, Natl Glycoengn Res Ctr, Jinan 250012, Shandong, Peoples R China
5.Shandong Acad Agr Sci, Inst Agrofood Sci Technol, Jinan 250100, Shandong, Peoples R China
关键词： Sulfated polysaccharide of Sepiella;maindroni ink;Matrix metalloproteinase-2;Epidermal growth factor receptor/p38;MAPK/PI3K/Akt/mTOR pathway
期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：6.953； 五年影响因子：6.737 ）
ISSN： 0141-8130
年卷期： 2018 年 107 卷
页码：
收录情况： SCI
摘要： Previous studies demonstrated that SIP-SII, a sulfated derivative of SIP that is isolated from the ink of Sepiella maindroni, showed significant inhibition of tumor growth and metastasis. In this study, the effects of SIP-SII on the migration, invasion and molecular mechanism in ovarian cancer cell line, SKOV-3 cells, were investigated. The flow cytometry, confocal microscope observation, western blot and RT-PCR results indicated that SIP-SII located on cell membrane and inhibited the expression and activation of epidermal growth factor receptor (EGFR). Moreover, the binding capacity of SIP-SII with EGFR was confirmed by surface plasmon resonance (SPR) analysis and co-localization of EGFR and SIP-SII. Accordingly, SIP-SII was proved to attenuate the EGF-induced EGFR phosphorylation and migration by western blot and wound healing assay, respectively. Additionally, SIP-SII inhibited p38/MAPK and PI3K/Akt/mTOR signaling pathways in SKOV-3 cells significantly. What is more, SIP-SII showed amplified inhibitory activity on migration, invasion, and MMP-2 expression in combination with p38-spedfic inhibitor, PI3K-specific inhibitor or mTOR-specific inhibitor in SKOV-3 cells. Therefore, the mechanism that SIP-SII suppressed EGFR-mediated p38/MAPK and PI3K/Akt/mT0R signaling pathways to inhibit migration and invasion of SKOV-3 cells was demonstrated. These findings suggested that SIP-SII might be used as a potential inhibitor against tumor metastasis. (C) 2017 Elsevier B.V. All rights reserved.
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