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首页> 外文期刊>Medical science monitor : >MicroRNA-200b Impacts Breast Cancer Cell Migration and Invasion by Regulating Ezrin-Radixin-Moesin
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MicroRNA-200b Impacts Breast Cancer Cell Migration and Invasion by Regulating Ezrin-Radixin-Moesin

机译:MicroRNA-200b通过调节Ezrin-Radixin-Moesin影响乳腺癌细胞迁移和侵袭

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BACKGROUND Ezrin-radixin-moesin (ERM) plays an important role in multiple links of tumors. It also involved in breast cancer invasion and metastasis, and might be a potential biomarker of breast cancer. Another study suggested that ERM expression was regulated directly by miR-200c, and had a critical role in miR-200c suppressing cell migration. This study aimed to investigate the effect of miR-200b on ERM expression in a breast cancer cell line and its influence on invasion and metastasis ability [i]in vitro[/i]. MATERIAL AND METHODS Breast cancer cell lines MCF-7 and MDA-MB-231 with different metastatic potentials were selected as a model. MiR-200b overexpression or inhibition was achieved by Lipofectamine? 2000-mediated miRNA transfection. RT-PCR was used to test miR-200b level, while Western blot was selected to detect ERM protein expression. Wound healing assay and Transwell assay were performed to determine cell migration and invasion ability. RESULTS RT-PCR revealed that miR-200b level in MDA-MB-231 was obviously lower than that in MCF-7, while Western blot analysis showed that ERM expression was significantly higher. MiR-200b inhibition by transfection in MCF-7 markedly decreased miR-200b level, elevated ERM expression, and enhanced cell migration and invasion. MiR-200b overexpression in MDA-MB-231 obviously increased miR-200b level, reduced ERM expression, and weakened cell migration and invasion. CONCLUSIONS MiR-200b participates in breast cancer cell migration and invasion through regulating ERM in MCF-7 and MDA-MB-231.
机译:背景技术Ezrin-radixin-moesin(ERM)在肿瘤的多个环节中起着重要的作用。它也参与乳腺癌的侵袭和转移,并且可能是乳腺癌的潜在生物标志物。另一项研究表明,ERM表达直接受miR-200c调节,在miR-200c抑制细胞迁移中起关键作用。这项研究旨在研究miR-200b对乳腺癌细胞系ERM表达的影响及其对体外侵袭和转移能力的影响[i]。材料与方法选择具有不同转移潜能的乳腺癌细胞MCF-7和MDA-MB-231作为模型。通过脂转染胺可以达到MiR-200b的过表达或抑制作用。 2000介导的miRNA转染。使用RT-PCR检测miR-200b水平,同时选择Western blot检测ERM蛋白表达。进行伤口愈合测定和Transwell测定以确定细胞迁移和侵袭能力。结果RT-PCR显示,MDA-MB-231中的miR-200b水平明显低于MCF-7,而Western blot分析显示ERM表达明显更高。在MCF-7中转染可抑制MiR-200b,从而显着降低miR-200b水平,ERM表达升高以及细胞迁移和侵袭增强。 MDA-MB-231中的MiR-200b过表达明显提高了miR-200b水平,降低了ERM表达,并减弱了细胞迁移和侵袭。结论MiR-200b通过调节MCF-7和MDA-MB-231中的ERM参与乳腺癌细胞的迁移和侵袭。

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