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Front Mol Neurosci:研究发现抗血管生成的通路或可成为成胶质细胞瘤的新靶点

2017-10-21 MedSci MedSci原创

成胶质细胞瘤(GBM)是发生于成年人的最具侵袭性的原发性颅内肿瘤,由于高度血管化的形成导致患者预后较差。因此,抗血管生成治疗已成为GBM治疗的一种有希望的治疗策略。本研究中,研究人员发现,胶质瘤样本和GBM细胞系中激活的T细胞5(NFAT5)的转录因子核因子水平明显升高,与胶质瘤WHO分级呈正相关。敲除NFAT5可抑制GBM细胞驱动的血管生成。此外,长链非编码RNA SBF2反义RNA 1(SBF

成胶质细胞瘤(GBM)是发生于成年人的最具侵袭性的原发性颅内肿瘤,由于高度血管化的形成导致患者预后较差。因此,抗血管生成治疗已成为GBM治疗的一种有希望的治疗策略。

本研究中,研究人员发现,胶质瘤样本和GBM细胞系中激活的T细胞5(NFAT5)的转录因子核因子水平明显升高,与胶质瘤WHO分级呈正相关。敲除NFAT5可抑制GBM细胞驱动的血管生成。此外,长链非编码RNA SBF2反义RNA 1(SBF2-AS1)在神经胶质瘤样本中上调,敲低SBF2-AS1可损害GBM诱导的血管生成。NFAT5的下调在转录水平上降低了SBF2-AS1的表达。

此外,SBF2-AS1的敲低通过增强miR-338-3p对EGF样 domain multiple 7(EGFL7)的抑制作用而抑制GBM细胞驱动的血管生成。体内研究表明,NFAT5敲低和SBF2-AS1敲低的组合产生最小的异种移植物体积和最低的微血管密度。

总之,该研究结果表明,NFAT5/SBF2-AS1/miR-338-3p/EGFL7途径可能为胶质瘤抗血管生成治疗提供新的靶点。

原始出处:

Hai Yu, Jian Zheng, et al., Transcription Factor NFAT5 Promotes Glioblastoma Cell-driven Angiogenesis via SBF2-AS1/miR-338-3p-Mediated EGFL7 Expression Change. Front Mol Neurosci. 2017; 10: 301. Published online 2017 Sep 21. doi: 10.3389/fnmol.2017.00301

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    2017-10-23 lsndxfj
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    2017-10-23 lsndxfj
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