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IFITM3/STAT3 轴促进神经胶质瘤细胞侵袭,受 TGF-β调节。

IFITM3/STAT3 axis promotes glioma cells invasion and is modulated by TGF-β.

机构信息

Department of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, 678 Fu Rong Road, Hefei, 230601, Anhui, China.

Cerebral Vascular Disease Research Center, Anhui Medical University, 678 Fu Rong Road, Hefei, 230601, Anhui, China.

出版信息

Mol Biol Rep. 2020 Jan;47(1):433-441. doi: 10.1007/s11033-019-05146-2. Epub 2019 Oct 21.

Abstract

Glioma is the most aggressive primary brain tumor. We have previously provided evidence that IFITM3 promoted glioma cells migration. However, the mechanism of how IFITM3 regulates glioma cells invasion and whether IFITM3 participates in TGF-β-mediated glioma invasion are still unknown. In this paper, we proved that IFITM3 was notably up-regulated in glioma tissues. Knockdown of IFITM3 suppressed STAT3 phosphorylation in vitro, and a specific STAT3 inhibitor AG490 reversed IFITM3-induced invasion of glioma cells. Furthermore, IFITM3 expression was induced by TGF-β in glioma and IFITM3 knockdown abolished TGF-β-mediated glioma cells invasion. Collectively, the results indicate that IFITM3/STAT3 axis may promote TGF-β-induced glioma cells invasion. This study provided some suggestions for the clinical treatment of the brain tumor.

摘要

神经胶质瘤是最具侵袭性的原发性脑肿瘤。我们之前已经提供了证据表明 IFITM3 促进了神经胶质瘤细胞的迁移。然而,IFITM3 如何调节神经胶质瘤细胞侵袭的机制以及 IFITM3 是否参与 TGF-β 介导的神经胶质瘤侵袭仍然未知。在本文中,我们证明 IFITM3 在神经胶质瘤组织中明显上调。IFITM3 的敲低抑制了体外 STAT3 的磷酸化,而特异性 STAT3 抑制剂 AG490 逆转了 IFITM3 诱导的神经胶质瘤细胞侵袭。此外,TGF-β 在神经胶质瘤中诱导 IFITM3 的表达,而 IFITM3 的敲低消除了 TGF-β 介导的神经胶质瘤细胞侵袭。总之,这些结果表明 IFITM3/STAT3 轴可能促进 TGF-β 诱导的神经胶质瘤细胞侵袭。本研究为脑肿瘤的临床治疗提供了一些建议。

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