微小RNA-200c通过靶向埃兹蛋白抑制神经胶质瘤的肿瘤进展。
MiR-200c Inhibits the Tumor Progression of Glioma via Targeting Moesin.
作者信息
Qin Yuanyuan, Chen Weilong, Liu Bingjie, Zhou Lei, Deng Lu, Niu Wanxiang, Bao Dejun, Cheng Chuandong, Li Dongxue, Liu Suling, Niu Chaoshi
机构信息
The CAS Key Laboratory of Innate Immunity and Chronic Disease, Hefei National Laboratory for Physical Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
Innovation Center for Cell Signaling Network.
出版信息
Theranostics. 2017 Apr 10;7(6):1663-1673. doi: 10.7150/thno.17886. eCollection 2017.
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 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.
我们试图证明miR-200c在胶质瘤进展中的调控作用及其背后的机制。在此，我们发现与瘤旁组织相比，miR-200c在胶质瘤组织中的表达显著降低，尤其是在恶性胶质瘤中。miR-200c的外源性过表达抑制了胶质瘤细胞的增殖和侵袭。此外，小鼠异种移植模型显示miR-200c抑制胶质瘤生长和肝转移，这主要是通过靶向埃兹蛋白（MSN）来调节的。我们证明胶质瘤标本中MSN的表达与miR-200c的表达呈负相关，并且MSN的过表达挽救了由miR-200c诱导的细胞增殖和侵袭表型。此外，敲低MSN能够模拟miR-200c在胶质瘤细胞中诱导的效应。这些结果表明miR-200c通过靶向MSN在胶质瘤的调控中发挥重要作用。
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