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长链非编码 RNA HAS2-AS1 通过作为竞争性内源 RNA 促进胶质母细胞瘤的肿瘤进展。

Long noncoding RNA HAS2-AS1 promotes tumor progression in glioblastoma via functioning as a competing endogenous RNA.

机构信息

Department of Neurology, Tianjin Neurological Institute, Key Laboratory of Post-Neurotrauma Neurorepair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China.

Department of Neurology, Xiqing Hospital, Tianjin, China.

出版信息

J Cell Biochem. 2020 Jan;121(1):661-671. doi: 10.1002/jcb.29313. Epub 2019 Aug 5.

DOI:10.1002/jcb.29313
PMID:31385362
Abstract

Glioblastoma multiforme (GBM) is a refractory tumor with poor prognosis and requires more effective treatment regimens. It has been confirmed that long noncoding RNAs (lncRNAs) substantially regulate various human disease including GBM. However, the biological roles and its underlying molecular mechanisms still need to be further investigated. In this study, the biological function and potential molecular mechanism of lncHAS2-AS1 in GBM were explored. It was discovered that HAS2-AS1 was elevated in glioma tissues and correlated with the prognosis of patients with glioma. Reduction of HAS2-AS1 suppressed the migration and invasion in vitro and in vivo. The transcription factor STAT1 could raise HAS2-AS1 by binding to its promoter region. Besides, HAS2-AS1 could adjust PRPS1 via sponging miR-608 in a direct manner. On the whole, the results of this study evidence that HAS2-AS1 is an oncogene and a potential therapeutic target for GBM.

摘要

多形性胶质母细胞瘤(GBM)是一种预后不良的难治性肿瘤,需要更有效的治疗方案。已经证实,长链非编码 RNA(lncRNA)在包括 GBM 在内的多种人类疾病中具有重要的调节作用。然而,其生物学功能及其潜在的分子机制仍需要进一步研究。在本研究中,探索了 lncHAS2-AS1 在 GBM 中的生物学功能和潜在的分子机制。研究发现,HAS2-AS1 在胶质瘤组织中上调,并与胶质瘤患者的预后相关。降低 HAS2-AS1 水平可抑制体外和体内的迁移和侵袭。转录因子 STAT1 可以通过结合其启动子区域来提高 HAS2-AS1 的表达。此外,HAS2-AS1 可以通过直接吸附 miR-608 来调节 PRPS1。总的来说,这项研究的结果表明,HAS2-AS1 是一种癌基因,是 GBM 的潜在治疗靶点。

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