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Research ArticlePROCEEDINGS OF THE CHINA-UNITED KINGDOM CANCER (CUKC) CONFERENCE, BEIJING, CHINA, 2017

Inhibition of Bevacizumab-induced Epithelial–Mesenchymal Transition by BATF2 Overexpression Involves the Suppression of Wnt/β-Catenin Signaling in Glioblastoma Cells

WENQIU HUANG, CHENGUANG ZHANG, MENGTIAN CUI, JING NIU and WEI DING
Anticancer Research August 2017, 37 (8) 4285-4294;
WENQIU HUANG
1Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China
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CHENGUANG ZHANG
1Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China
2Beijing Key Laboratory for Researches in Cancer Invasion and Metastasis, Cancer Institute of Capital Medical University, Beijing, P.R. China
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MENGTIAN CUI
1Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China
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JING NIU
1Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China
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WEI DING
1Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China
2Beijing Key Laboratory for Researches in Cancer Invasion and Metastasis, Cancer Institute of Capital Medical University, Beijing, P.R. China
3Beijing Institute of Brain Disorders, Beijing, P.R. China
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  • For correspondence: weiding@ccmu.edu.cn
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Abstract

Background/Aim: Bevacizumab (BV) has been used for the treatment of recurrent glioblastoma. However, it also induces epithelial–mesenchymal transition (EMT) in glioblastoma cells, which compromises its efficacy. BATF2 (basic leucine zipper ATF-like transcription factor 2), a multi-target transcriptional repressor, has been found to suppress cancer development partly through inhibition of Wnt/β-catenin singling. The roles of BATF2 and Wnt/β-catenin signaling in BV-induced EMT in glioblastoma cells were investigated in this study. Materials and Methods: BV was used to treat U87MG cells, and TOP/FOP FLASH luciferase reporters were employed to determine the activity of Wnt/β-catenin signaling. EMT markers were detected with quantitative reverse transcription-PCR and western blotting. Immunofluorescence (IF) was used to determine the compartmentation of β-catenin. Wound-healing, TransWell and ECIS assays were used to analyze cell adhesion, invasion and migration. Results: BV induced EMT phenotype in U87MG cells, and BATF2 overexpression significantly inhibited BV-induced EMT with suppression of Wnt/β-catenin signaling. Conclusion: Our findings expanded the understanding of the role of BATF2 in tumors, and also suggested a potential of using BATF2 as a therapeutic target to hinder bevacizumab induced EMT in glioblastoma.

  • Glioblastoma
  • BATF2
  • EMT
  • Wnt/β-catenin
  • Received May 19, 2017.
  • Revision received June 9, 2017.
  • Accepted June 12, 2017.
  • Copyright© 2017, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved
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August 2017
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Inhibition of Bevacizumab-induced Epithelial–Mesenchymal Transition by BATF2 Overexpression Involves the Suppression of Wnt/β-Catenin Signaling in Glioblastoma Cells
WENQIU HUANG, CHENGUANG ZHANG, MENGTIAN CUI, JING NIU, WEI DING
Anticancer Research Aug 2017, 37 (8) 4285-4294;

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Inhibition of Bevacizumab-induced Epithelial–Mesenchymal Transition by BATF2 Overexpression Involves the Suppression of Wnt/β-Catenin Signaling in Glioblastoma Cells
WENQIU HUANG, CHENGUANG ZHANG, MENGTIAN CUI, JING NIU, WEI DING
Anticancer Research Aug 2017, 37 (8) 4285-4294;
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Keywords

  • glioblastoma
  • BATF2
  • EMT
  • Wnt/β-catenin
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