Abstract:
: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 withSTAT1inhibitors. 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. SIGNIFICANCE OF THE STUDY: Glioblastoma is one of the most malignant tumors with very high mortality. Until now, there is no efficient therapy against glioblastoma. In this study, we found downregulation of Signal transducer and activator of transcription 1 (STAT1) could weaken the aggressiveness of glioblastoma cells through inhibition in epithelial-mesenchymal transition, mediated through wnt/β-catenin signalling pathway. Thus, this work supported the regulatory role of STAT1 in glioblastoma growth and migration. This potentially serves as a new therapeutic target against glioblastoma.
journal_name
Cell Biochem Functjournal_title
Cell biochemistry and functionauthors
Zhao L,Li X,Su J,Wang Gong F,Lu J,Wei Ydoi
10.1002/cbf.3518subject
Has Abstractpub_date
2020-07-01 00:00:00pages
630-641issue
5eissn
0263-6484issn
1099-0844journal_volume
38pub_type
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