miR-603 通过抑制 WIF1 和 CTNNBIP1 促进胶质瘤细胞生长通过 Wnt/β-catenin 通路。
miR-603 promotes glioma cell growth via Wnt/β-catenin pathway by inhibiting WIF1 and CTNNBIP1.
机构信息
Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, China.
Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, China; Department of Medical Service Management, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, China.
出版信息
Cancer Lett. 2015 Apr 28;360(1):76-86. doi: 10.1016/j.canlet.2015.02.003. Epub 2015 Feb 10.
Gliomas are the most common and deadly type of brain tumor. In spite of progressive treatments, patient prognosis has not improved significantly. MicroRNAs are considered promising candidates for glioma therapy. MiR-603 was found overexpressed in both glioma tissues and cell lines. MiR-603 promoted cell proliferation, cell cycle progression and neurosphere formation. Conversely, inhibition of miR-603 remarkably reduced these effects. We confirmed that WIF1 and CTNNBIP1 are bona fide targets of miR-603. The negative correlation between miR-603 and these molecules' expression was shown by Pearson correlation in 50 primary glioma tissue samples. Furthermore, overexpression of miR-603 promoted nuclear β-catenin levels and TOPflash luciferase activity, indicating that miR-603 activates the Wnt/β-catenin signaling pathway. Our in vivo results confirmed the positive role of miR-603 in glioma development. We demonstrate that miR-603 regulates glioma development via its WIF1 and CTNNBIP1 targets, which suggests that miR-603 may be a promising candidate for therapeutic applications in glioma treatment.
神经胶质瘤是最常见和最致命的脑肿瘤类型。尽管进行了不断的治疗，但患者的预后并没有显著改善。microRNAs 被认为是神经胶质瘤治疗的有前途的候选物。miR-603 在神经胶质瘤组织和细胞系中均过度表达。miR-603 促进细胞增殖、细胞周期进程和神经球形成。相反，抑制 miR-603 显著降低了这些效果。我们证实 WIF1 和 CTNNBIP1 是 miR-603 的真正靶标。在 50 个原发性神经胶质瘤组织样本中，通过 Pearson 相关性分析显示 miR-603 与这些分子表达之间存在负相关。此外，miR-603 的过表达促进了核 β-catenin 水平和 TOPflash 荧光素酶活性，表明 miR-603 激活了 Wnt/β-catenin 信号通路。我们的体内结果证实了 miR-603 在神经胶质瘤发展中的积极作用。我们证明 miR-603 通过其 WIF1 和 CTNNBIP1 靶标调节神经胶质瘤的发展，这表明 miR-603 可能是神经胶质瘤治疗中治疗应用的有前途的候选物。
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