A Novel Selenadiazole Derivative Induces Apoptosis in Human Glioma Cells by Dephosphorylation of AKT

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  • Zhang Yikai
    Guangdong Province Key Laboratory of Molecule Immunology and Antibody Engineering, Department of Pathology, Jinan University
  • Zheng Shanyuan
    School of Life Sciences and State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong
  • Ngai Sai-Ming
    School of Life Sciences and State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong
  • Zheng Wenjie
    Department of Chemistry, Jinan University
  • Li Jinying
    Guangdong Province Key Laboratory of Molecule Immunology and Antibody Engineering, Department of Pathology, Jinan University
  • Chen Tianfeng
    Department of Chemistry, Jinan University
  • Zhong Xueyun
    Guangdong Province Key Laboratory of Molecule Immunology and Antibody Engineering, Department of Pathology, Jinan University

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Selenadiazole derivatives are synthetic organoselenium compounds with improved anticancer activity and greater selectivity than inorganic selenium. In this study, 4-(benzo[c][1,2,5]selenadiazol-6-yl)-benzene-1,2-diamine (BSBD) was shown to induce time- and dose-dependent apoptosis in SWO-38 human glioma cells by accumulation of a sub-G1 cell population, DNA fragmentation, nuclear condensation, caspase activation and poly(ADP-ribose) polymerase (PARP) cleavage. Further mechanistic investigation showed that BSBD treatment induced dephosphorylation of AKT and DNA damage-mediated activation of p53, leading to extensive apoptosis through the mitochondrial pathway. Our findings suggest that BSBD represents a potential human glioma therapeutic.

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