Suppr超能文献

曼氏无针乌贼墨多糖通过抑制 EGFR 介导的 p38/MAPK 和 PI3K/Akt/mTOR 信号通路抑制 SKOV-3 细胞的迁移、侵袭和基质金属蛋白酶-2 的表达。

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.

机构信息

Key Laboratory of Chemical Biology (Ministry of Education), Institute of Biochemical and Biotechnological Drugs, School of Pharmaceutical Sciences, Shandong University, Jinan 250012, Shandong, PR China.

Department of Pharmacology, School of Pharmaceutical Sciences, Shandong University, Jinan 250012, Shandong, PR China.

出版信息

Int J Biol Macromol. 2018 Feb;107(Pt A):349-362. doi: 10.1016/j.ijbiomac.2017.08.178. Epub 2017 Sep 9.

Abstract

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-specific 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/mTOR 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.

摘要

先前的研究表明,SIP-SII 是从墨鱼墨囊中分离得到的 SIP 的硫酸化衍生物,对肿瘤生长和转移具有显著的抑制作用。本研究旨在探讨 SIP-SII 对卵巢癌细胞系 SKOV-3 迁移、侵袭的影响及其分子机制。流式细胞术、共聚焦显微镜观察、Western blot 和 RT-PCR 结果表明,SIP-SII 位于细胞膜上,抑制表皮生长因子受体(EGFR)的表达和激活。此外,表面等离子体共振(SPR)分析和 EGFR 与 SIP-SII 的共定位证实了 SIP-SII 与 EGFR 的结合能力。因此,通过 Western blot 和划痕愈合实验分别证实了 SIP-SII 可减弱 EGF 诱导的 EGFR 磷酸化和迁移。此外,SIP-SII 还显著抑制了 SKOV-3 细胞中 p38/MAPK 和 PI3K/Akt/mTOR 信号通路。更重要的是,SIP-SII 与 p38 特异性抑制剂、PI3K 特异性抑制剂或 mTOR 特异性抑制剂联合使用时,在 SKOV-3 细胞中对迁移、侵袭和 MMP-2 表达的抑制作用增强。因此,SIP-SII 通过抑制 EGFR 介导的 p38/MAPK 和 PI3K/Akt/mTOR 信号通路来抑制 SKOV-3 细胞的迁移和侵袭的机制得到了证实。这些发现表明,SIP-SII 可能作为一种潜在的肿瘤转移抑制剂。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验