hsa-miR-9 controls the mobility behavior of glioblastoma cells via regulation of MAPK14 signaling elements.
hsa-miR-9 controls the mobility behavior of glioblastoma cells via regulation of MAPK14 signaling elements.
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DOI：
10.18632/oncotarget.6687
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发表时间：
2016-04-26
期刊：
影响因子：
--
通讯作者：
Efroni S
中科院分区：
文献类型：
--
作者：
Ben-Hamo R;Zilberberg A;Cohen H;Efroni S
多形性胶质母细胞瘤(GBM)是脑部最常见、最致命的原发肿瘤。尽管在不同的治疗模式上做了很多努力，但基底膜与所有人类癌症中最差的5年生存率之一有关。在这里，我们展示了特定的GBM癌症表型，这些表型由MAPAKAP网络的修改所控制。然后，我们展示了一种新的调控模式，通过该模式，MAPKAP途径的一组五个关键因子由相同的microRNA hsa-miR-9调控。我们证明hsa-miR-9过表达导致MAPKAP信号抑制，部分是通过干扰MAPK14/MAPKAP3复合体。此外，hsa-miR-9的过表达启动了肌动蛋白细丝的重新排列，这导致我们假设了观察到的表型转变的机制。这项工作揭示了新的microRNA特征，并将hsa-miR-9定位为治疗靶点，它通过MAPKAP信号调节转移，从而决定GBM的预后。
Glioblastoma Multiforme (GBM) is the most common and lethal primary tumor of the brain. GBM is associated with one of the worst 5-year survival rates among all human cancers, despite much effort in different modes of treatment. Here, we demonstrate specific GBM cancer phenotypes that are governed by modifications to the MAPAKAP network. We then demonstrate a novel regulation mode by which a set of five key factors of the MAPKAP pathway are regulated by the same microRNA, hsa-miR-9. We demonstrate that hsa-miR-9 overexpression leads to MAPKAP signaling inhibition, partially by interfering with the MAPK14/MAPKAP3 complex. Further, hsa-miR-9 overexpression initiates re-arrangement of actin filaments, which leads us to hypothesize a mechanism for the observed phenotypic shift. The work presented here exposes novel microRNA features and situates hsa-miR-9 as a therapeutic target, which governs metastasis and thus determines prognosis in GBM through MAPKAP signaling.
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影响因子：
14.9
作者：
Chen C;Ridzon DA;Broomer AJ;Zhou Z;Lee DH;Nguyen JT;Barbisin M;Xu NL;Mahuvakar VR;Andersen MR;Lao KQ;Livak KJ;Guegler KJ
通讯作者：
Guegler KJ
影响因子：
4.1
作者：
ANZIL, AP
通讯作者：
ANZIL, AP
影响因子：
5.8
作者：
Ben-Hamo, Rotem;Gidoni, Moriah;Efroni, Sol
通讯作者：
Efroni, Sol
影响因子：
11.2
作者：
Kefas, Benjamin;Godlewski, Jakub;Purow, Benjamin
通讯作者：
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影响因子：
4.1
作者：
ELGINDI, S;SALAMA, M;FARAG, S
通讯作者：
FARAG, S