| Literature DB >> 29800921 |
Yunsheng Zhang1, Guishan Jin2, Junwen Zhang2, Ruifang Mi2, Yiqiang Zhou2, Wenhua Fan2, Sen Cheng2, Wenjie Song2, Bo Zhang2, Mengjiao Ma2, Fusheng Liu3.
Abstract
Hypoxia is common in Glioblastoma (GBM). By regulating the 'hypoxia signaling cascade', hypoxia affects several processes including cell proliferation, invasion, and angiogenesis. Some studies have revealed that signal transducer and activator of transcription (STAT), including STAT1, is abnormal under hypoxia in several cancers. Here, we investigated the role of STAT1 under hypoxia in glioma progression. We found that STAT1 was downregulated under a hypoxic condition in U251 and U373. STAT1 overexpression can not only decrease proliferation, migration and invasion in U251 and U373 but also inhibit tube formation of HBMECs. Moreover, overexpression of STAT1 decreased tumor growth and prolonged the overall survival of xenograft mice. We also showed that STAT1 overexpression inhibited the expression of HIF-1α and VEGF-A. Our work suggests that STAT1 plays a pivotal role as a tumor suppressor in glioma under hypoxia, and it could be a potential new therapeutic target in glioma.Entities:
Keywords: Glioblastoma multiforme; Hypoxia-inducible factor-1α; Signal transducer and activator of transcription; Vascular endothelial growth factor A
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Year: 2018 PMID： 29800921 DOI： 10.1016/j.biopha.2018.05.079
Source DB: PubMed Journal: Biomed Pharmacother ISSN： 0753-3322 Impact factor: 6.529