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首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >High mannose N-glycan binding lectin from Remusatia vivipara (RVL) limits cell growth, motility and invasiveness of human breast cancer cells
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High mannose N-glycan binding lectin from Remusatia vivipara (RVL) limits cell growth, motility and invasiveness of human breast cancer cells

机译:来自饲养雷帕拉(RVL)的高甘露甘草结合凝集凝集素(RVL)限制了人乳腺癌细胞的细胞生长,运动和侵袭性

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Breast cancer known for its high metastatic potential is responsible for large mortality rate amongst women; hence it is imperative to search for effective anti-metastatic molecules despite anticancer drugs. The current study describes the potential of Remusatia vivipara lectin (RVL), inducing apoptosis in breast cancer cells there by limiting motility and invasiveness. RVL binds to the cell surface glycans of MDA-MB468 and MCF-7 cells, exhibiting strong glycan mediated cytotoxic effect, but show marginal effect on non-tumorigenic MCF-10A cells. RVL elicits increased cellular stress, apoptotic vacuoles and nuclear disintegration in both MDA-MB-468 and MCF-7 cells accompanied by depletion of G0/G1, S and G2/M phases. Lectin interaction induced production of reactive oxygen species through altering mitochondrial membrane potential progressing to apoptosis. Further, RVL strongly elicited reproductive cell death in MDA-MB-468 cells and showed strong inhibitory effect on neovascularization demonstrated in chorioallantoic membrane assay. Treatment of MDA-MB-468 cells with RVL, suppress the motility and invasive property as shown by scratch wound heal and Boyden chamber transwell assays respectively. These results provide an insight into significance of interaction of RVL with specific cell surface high mannose N-glycans resulting in curtailing the metastatic ability of cancer cells. (C) 2017 Elsevier Masson SAS. All rights reserved.
机译:以其高转移性潜力而闻名的乳腺癌负责女性中的大死亡率;因此,尽管存在抗癌药物,因此必须寻找有效的抗转移分子。目前的研究描述了雷帕氏菌凝集素(RVL)的潜力,通过限制动力和侵袭性诱导乳腺癌细胞中的凋亡。 RV1与MDA-MB468和MCF-7细胞的细胞表面聚糖结合,表现出强甘草介导的细胞毒性作用,但在非致瘤MCF-10A细胞上显示了边缘效应。 RVL引发了MDA-MB-468和MCF-7细胞中的细胞应激,凋亡液泡和核崩解,伴随着G0 / G1,S和G2 / M相的耗尽。通过改变对细胞凋亡的线粒体膜电位改变线粒体膜电位,凝集素相互作用诱导活性氧物质的产生。此外,RVL在MDA-MB-468细胞中强烈引起的生殖细胞死亡,并对细胞囊膜膜测定中显示的新血管形成表现出强烈的抑制作用。用RV1处理MDA-MB-468细胞,抑制刮伤伤口愈合和Boyden室Transwell测定所示的运动和侵袭性。这些结果熟悉RVL与特定细胞表面高甘露糖N-聚糖的重要性的重要性,导致缩短癌细胞的转移能力。 (c)2017年Elsevier Masson SAS。版权所有。

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