Paired related homeobox 1 is associated with the invasive properties of glioblastoma cells.

Paired related homeobox 1 is associated with the invasive properties of glioblastoma cells.
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DOI:
10.3892/or.2014.3681
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发表时间:
2015-03
期刊:
影响因子:
4.2
通讯作者:
Mai Sugiyama;Hitoki Hasegawa;S. Ito;Kazuya Sugiyama;Masao Maeda;Kosuke Aoki;T. Wakabayashi;M. Hamaguchi;A. Natsume;T. Senga
Mai Sugiyama;Hitoki Hasegawa;S. Ito;Kazuya Sugiyama;Masao Maeda;Kosuke Aoki;T. Wakabayashi;M. Hamaguchi;A. Natsume;T. Senga
中科院分区:
医学3区
文献类型:
--
作者:
Mai Sugiyama;Hitoki Hasegawa;S. Ito;Kazuya Sugiyama;Masao Maeda;Kosuke Aoki;T. Wakabayashi;M. Hamaguchi;A. Natsume;T. Senga

文献摘要

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胶质母细胞瘤是一种高度增殖性和侵袭性的肿瘤。尽管为开发胶质母细胞瘤的治疗方法付出了巨大的努力,但目前可用的疗法效果有限。为了开发胶质母细胞瘤治疗的新策略,阐明促进胶质母细胞瘤侵袭特性的分子机制至关重要。在本研究中,我们发现配对相关同源盒 1 (PRRX1) 与胶质母细胞瘤细胞侵袭相关。 PRRX1 的缺失抑制了胶质母细胞瘤细胞的侵袭和神经球形成。相反,PRRX1的外源表达促进侵袭。 Notch信号通路是一条进化上保守的通路,对于发育过程至关重要,在胶质母细胞瘤的肿瘤发生中发挥着重要作用。 PRRX1的表达诱导Notch信号的激活,而Notch信号的抑制则抑制了PRRX1介导的细胞侵袭。我们的结果表明 PRRX1 激活 Notch 信号传导与促进胶质母细胞瘤细胞侵袭有关。
Glioblastoma is a highly proliferative and invasive tumor. Despite extensive efforts to develop treatments for glioblastoma, the currently available therapies have only limited effects. To develop novel strategies for glioblastoma treatment, it is crucial to elucidate the molecular mechanisms that promote the invasive properties of glioblastoma. In the present study, we showed that the paired related homeobox 1 (PRRX1) is associated with glioblastoma cell invasion. The depletion of PRRX1 suppressed the invasion and neurosphere formation of glioblastoma cells. Conversely, the exogenous expression of PRRX1 promoted invasion. The Notch signaling pathway, which is an evolutionarily conserved pathway that is essential for developmental processes, plays an important role in the tumorigenesis of glioblastoma. The expression of PRRX1 induced the activation of Notch signaling, and the inhibition of Notch signaling suppressed PRRX1-mediated cell invasion. Our results indicate that activation of Notch signaling by PRRX1 is associated with the promotion of glioblastoma cell invasion.