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Retracted: Glabridin attenuates the migratory and invasive capacity of breast cancer cells by activating microRNA‐200c

机译:缩回:格列本汀通过激活microRNA-200c减弱乳腺癌细胞的迁移和侵袭能力

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AbstractCurrent treatments for breast cancer, a common malignancy in human females, are less than satisfactory because of high rates of metastasis. Glabridin (GLA), which acts through the FAK/ROS signaling pathway, has been used as an antioxidant and anti-metastatic agent. However, little is known regarding the effect of microRNA (miRNA) on GLA's anti-metastatic activity. The miRNA-200 family, which is frequently expressed at low levels in triple negative breast cancers, inhibits metastasis by blocking the epithelial–mesenchymal transition. Here, we found that GLA attenuated the migratory and invasive capacity of breast cancer cells by activating miR-200c. GLA induced the mesenchymal–epithelial transition in vitro and in vivo, as determined by increased expression of the epithelial marker, E-cadherin, and decreased expression of the mesenchymal marker, vimentin. Overexpression of miR-200c enhanced the expression of E-cadherin and decreased the expression of vimentin. Furthermore, in MDA-MB-231 and BT-549 breast cancer cells exposed to GLA, knockdown of miR-200c blocked the GLA-induced mesenchymal–epithelial transition and alleviated the GLA-induced inhibition of migration and invasion. Thus, elevation of miR-200c by GLA has considerable therapeutic potential for anti-metastatic therapy for breast cancer patients.
机译:摘要由于乳腺癌的高转移率,目前用于治疗乳腺癌(一种常见于女性的恶性肿瘤)的方法并不令人满意。通过FAK / ROS信号通路起作用的格拉布里定(GLA)已被用作抗氧化剂和抗转移剂。但是,关于microRNA(miRNA)对GLA的抗转移活性的影响知之甚少。 miRNA-200家族在三阴性乳腺癌中经常以低水平表达,通过阻断上皮-间质转化抑制转移。在这里,我们发现GLA通过激活miR-200c减弱了乳腺癌细胞的迁移和侵袭能力。 GLA在体外和体内均可诱导间充质-上皮转化,这取决于上皮标记物E-钙黏着蛋白的表达增加和间质标记物波形蛋白的表达减少。 miR-200c的过表达增强E-钙黏着蛋白的表达,降低波形蛋白的表达。此外,在暴露于GLA的MDA-MB-231和BT-549乳腺癌细胞中,敲低miR-200c阻断了GLA诱导的间充质-上皮转化,并减轻了GLA诱导的迁移和侵袭抑制。因此,通过GLA升高miR-200c对于乳腺癌患者的抗转移疗法具有相当大的治疗潜力。

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