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IGFBP5 increases cell invasion and inhibits cell proliferation by EMT and Akt signaling pathway in Glioblastoma multiforme cells

机译：IGFBP5增加细胞侵袭并抑制EMT和AKT信号通路在胶质母细胞瘤多形细胞中的细胞增殖

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Recurrence of Glioblastoma multiforme (GBM) seems to be the rule despite combination therapies. Cell invasion and cell proliferation are major reasons for recurrence of GBM. And insulin-like growth factor binding protein 5 (IGFBP5) is the most conserved of the IGFBPs and is frequently dysregulated in cancers and metastatic tissues. By studying the human glioma tissues, we find that IGFBP5 expression associate to the histopathological classification and highly expressed in GBM. Using IGFBP5 mutants we demonstrate that knockdown of IGFBP5 inhibited cell invasion, whereas promoting cell proliferation in GBM cells. Mechanistically, we observed that promoting GBM cell proliferation by inhibiting IGFBP5 was associated with stimulating Akt (Protein kinase B) phosphorylation. However, IGFBP5 promote GBM cell invasion was related to the epithelial-to-mesenchymal transition (EMT). Furthermore, the Chinese Glioma Genome Altas (CGGA) database show that IGFBP5 is significantly increased in recurrent glioma and it predicted worse survival. The obtained results indicate that IGFBP5 has two sides in GBM—inhibiting cell proliferation but promoting cell invasion.
机译：尽管组合疗法，胶质母细胞瘤的复发似乎是规则。细胞浸润和细胞增殖是GBM复发的主要原因。和胰岛素样生长因子结合蛋白5（IGFBP5）是IGFBP中最保守的，并且经常在癌症和转移组织中进行过度消退。通过研究人胶质瘤组织，我们发现IGFBP5表达与组织病理学分类有关，并且在GBM中表达高度表达。使用IGFBP5突变体，我们证明了IGFBP5的敲低抑制细胞侵袭，而促进GBM细胞中的细胞增殖。机械地，我们观察到通过抑制IGFBP5促进GBM细胞增殖与刺激AKT（蛋白激酶B）磷酸化有关。然而，IGFBP5促进GBM细胞侵袭与上皮 - 间充质转换（EMT）有关。此外，中国胶质瘤基因组ALTAS（CGGA）数据库表明，在经常性胶质瘤中，IGFBP5显着增加，预测存活率更差。所得结果表明IGFBP5在GBM抑制细胞增殖中具有两侧，但促进细胞侵袭。

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