Yongzhi Lu,1 Wei Sun,2 Liang Zhang,3 Junyao Li4

1Department of Oncology, Qingdao Municipal Hospital, Qingdao, Shandong Province 266000, Peoples Republic of China; 2Department of Neurology, Qingdao Third Peoples Hospital, Qingdao, Shandong Province 266000, Peoples Republic of China; 3Department of Critical Care Medicine, Qingdao Eighth Peoples Hospital, Qingdao, Shandong Province 266000, Peoples Republic of China; 4Department of Emergency, Qingdao Municipal Hospital, Qingdao, Shandong Province 266000, Peoples Republic of China

Correspondence: Junyao LiDepartment of Emergency, Qingdao Municipal Hospital, Qingdao, Shandong Province 266000, Peoples Republic of ChinaEmail wmy_188@126.com

Background: Membrane-associated guanylate kinase (MAGUK) with inverted orientation protein 1 (MAGI1) is a novel member of the MAGUK family with a vital role in tumor progression related to invasion and metastasis. However, the function of MAGI1 in glioma is currently unknown. We therefore analyzed the expression of MAGI1 protein in human glioma samples, glioma cell lines and glioma stem cells (GSCs), and explored its effects on glioma cell proliferation and apoptosis.Methods: MAGI1 expression in glioma tissues was examined by Western blotting and real-time polymerase chain reaction and its relationships with clinical pathological features were analyzed. The effects of MAGI1 knockdown on the proliferation of glioma cell lines and GSCs were detected by CCK8 and colony-formation assays, and apoptosis was assessed by flow cytometry. We also investigated the effects of MAGI1 silencing on protein expression levels of epithelial-mesenchymal transition biomarkers, as well as -catenin, cyclin D1, PTEN and phospho-Akt by Western blotting.Results: MAGI1 was significantly downregulated in glioma tissues and its expression was related to cancer progression. Silencing of MAGI1 in both glioma cell lines and GSCs enhanced proliferation and inhibited apoptosis. MAGI1 knockdown also significantly increased the expression levels of N-cadherin, vimentin, -catenin, cyclin D1 and phospho-Akt and reduced the expression of E-cadherin and PTEN.Conclusions: Our results indicated that MAGI1 might play a vital role in glioma progression and may represent a potential therapeutic target for the treatment of glioma.

Keywords: glioma, MAGI1, -catenin, EMT, proliferation, knockdown

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