We attempt to demonstrate the regulatory role of miR-200c in glioma progression and its mechanisms behind. Here, we show that miR-200c expression was significantly reduced in the glioma tissues compared to paratumor tissues, especially in malignant glioma. Exogenous overexpression of miR-200c inhibited the proliferation and invasion of glioma cells. In addition, the in vivo mouse xenograft model showed that miR-200c inhibited glioma growth and liver metastasis, which is mainly regulated by targeting moesin (MSN). We demonstrated that the expression of MSN in glioma specimens were negatively correlated with miR-200c expression, and MSN overexpression rescued the phenotype about cell proliferation and invasion induced by miR-200c. Moreover, knockdown of MSN was able to mimic the effects induced by miR-200c in glioma cells. These results indicate that miR-200c plays an important role in the regulation of glioma through targeting MSN.

中文翻译：

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MiR-200c通过靶向肌动蛋白抑制胶质瘤的肿瘤进展

我们试图证明miR-200c在神经胶质瘤进展中的调控作用及其背后的机制。在这里，我们显示，与癌旁组织相比，神经胶质瘤组织中miR-200c表达显着降低，尤其是在恶性神经胶质瘤中。miR-200c的外源性过表达抑制神经胶质瘤细胞的增殖和侵袭。另外，体内小鼠异种移植模型显示，miR-200c抑制神经胶质瘤的生长和肝转移，这主要是通过靶向肌球蛋白（MSN）来调节的。我们证明神经胶质瘤标本中的MSN的表达与miR-200c的表达呈负相关，而MSN的过表达挽救了miR-200c诱导的细胞增殖和侵袭的表型。而且，敲低MSN能够模拟神经胶质瘤细胞中miR-200c诱导的作用。这些结果表明，miR-200c通过靶向MSN在神经胶质瘤的调节中起着重要作用。