Glioblastoma is one of the most malignant tumors and causes the high mortality in cancer patients. Currently, there is no highly efficient therapy against glioblastoma. Therefore, searching for a new molecular target to anti‐glioblastoma therapy is urgent and necessary. In this study, we elucidated the role of Signal transducer and activator of transcription 1 (STAT1 ) in proliferation, migration and apoptosis of glioblastoma cells. We found that STAT1 downregulation could weaken the aggressiveness of glioblastoma cells. Besides, the glioblastoma growth in vivo was also inhibited with the STAT1 downregulation by shRNA as well as by pharmacological stimulation withSTAT1 inhibitors. This negative regulation of tumor growth was accompanied by the inhibition in epithelial‐mesenchymal transition (EMT), whereas the STAT1 overexpression promoted EMT. Furthermore, the involvement of wnt/β‐catenin was observed in STAT1 downregulation mediated weakness in glioblastoma aggressiveness since application of activator wnt agonist 1 could counteract the inhibitory effect induced by STAT1 downregulation. Collectively, this work provided the evidence to support the conclusion that STAT1 can regulate the glioblastoma growth and migration, potentially serving as a therapeutic target against glioblastoma.

中文翻译：

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STAT1通过wnt /β-catenin信号传导途径确定胶质母细胞瘤在体内和体外的侵袭性。

胶质母细胞瘤是最恶性的肿瘤之一，并导致癌症患者的高死亡率。当前，没有针对胶质母细胞瘤的高效疗法。因此，寻找抗胶质母细胞瘤治疗的新分子靶标迫在眉睫。在这项研究中，我们阐明了信号转导子和转录激活子1（STAT1）在胶质母细胞瘤细胞增殖，迁移和凋亡中的作用。我们发现STAT1的下调可能会削弱胶质母细胞瘤细胞的侵略性。此外，shRNA以及STAT1的药理刺激也抑制了STAT1的表达，从而抑制了胶质母细胞瘤的体内生长。抑制剂。肿瘤生长的这种负调节伴随着上皮-间质转化（EMT）的抑制，而STAT1过表达促进了EMT。此外，由于应用激活剂wnt激动剂1可以抵消STAT1下调诱导的抑制作用，因此在STAT1下调介导的胶质母细胞瘤侵袭性弱点中观察到了wnt /β-catenin的参与。总的来说，这项工作提供了证据来支持STAT1可以调节胶质母细胞瘤的生长和迁移的结论，并有可能作为针对胶质母细胞瘤的治疗靶标。