首页> 美国卫生研究院文献>Brazilian Journal of Medical and Biological Research >Astragalus polysaccharides decrease proliferation migration and invasion but increase apoptosis of human osteosarcoma cells by up-regulation of microRNA-133a
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Astragalus polysaccharides decrease proliferation migration and invasion but increase apoptosis of human osteosarcoma cells by up-regulation of microRNA-133a

机译:黄芪多糖通过上调microRNA-133a减少人骨肉瘤细胞的增殖迁移和侵袭但增加其凋亡

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摘要

Osteosarcoma (OS) has a high incidence, malignity, and frequency of recurrence and metastasis. In this study, we aimed to explore the potential anti-cancer effects of Astragalus polysaccharides (APS) on human OS MG63 cells as well as underlying mechanisms. Viability of MG63 cells was assessed by CCK-8 assay to determine the adequate concentration of APS. Then, effects of APS on MG63 cell proliferation, cell cycle distribution, apoptosis, and migration and invasion were analyzed by BrdU incorporation, PI staining, flow cytometry, and transwell assays, respectively. The expression levels of proteins involved in these physiological processes were assessed by western blot analysis. Afterwards, miR-133a level in APS-treated cells was determined by qRT-PCR, and whether APS affected MG63 cells through regulation of miR-133a was determined. Finally, the activation of c-Jun N-terminal protein kinase (JNK) pathway was detected. We found that APS treatment suppressed the viability, proliferation, migration, and invasion of MG63 cells, as well as induced cell apoptosis. Moreover, APS enhanced the expression of miR-133a in MG63 cells. Knockdown of miR-133a reversed the APS treatment-induced MG63 cell proliferation, migration and invasion inhibition, as well as cell apoptosis. Furthermore, APS inactivated JNK pathway in MG63 cells. Knockdown of miR-133a reversed the APS treatment-induced inactivation of JNK pathway in MG63 cells. To conclude, APS repressed proliferation, migration, and invasion while induced apoptosis of OS MG63 cells by up-regulating miR-133a and then inactivating JNK pathway.
机译:骨肉瘤(OS)的发生率,恶性程度高,复发和转移的频率也高。在这项研究中,我们旨在探讨黄芪多糖(APS)对人OS MG63细胞的潜在抗癌作用及其潜在机制。通过CCK-8分析评估MG63细胞的活力,以确定足够的APS浓度。然后,分别通过BrdU掺入,PI染色,流式细胞术和transwell分析法分析了APS对MG63细胞增殖,细胞周期分布,细胞凋亡以及迁移和侵袭的影响。通过蛋白质印迹分析评估参与这些生理过程的蛋白质的表达水平。之后,通过qRT-PCR确定APS处理的细胞中的miR-133a水平,并确定APS是否通过调节miR-133a来影响MG63细胞。最后,检测到c-Jun N端蛋白激酶(JNK)途径的激活。我们发现,APS处理抑制了MG63细胞的活力,增殖,迁移和侵袭,并诱导了细胞凋亡。此外,APS增强了MG63细胞中miR-133a的表达。抑制miR-133a逆转了APS治疗诱导的MG63细胞增殖,迁移和侵袭抑制以及细胞凋亡。此外,APS使MG63细胞中的JNK途径失活。抑制miR-133a逆转了APS治疗诱导的MG63细胞JNK途径失活。总之,APS通过上调miR-133a然后失活JNK途径抑制OS MG63细胞的增殖,迁移和侵袭,同时诱导OS MG63细胞凋亡。

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