Ying Yu1, Bo Yang2, Jinlu Yu1, Gang Zhao1, Fan Chen3. 1. Department of Neurosurgery, The First Hospital of Jilin University, 71 Xinmin Avenue, Changchun, Jilin, 130021, China. 2. Department of Hematology, The second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, 28 Fuxing Road, Beijing, 100853, China. 3. Department of Neurosurgery, The First Hospital of Jilin University, 71 Xinmin Avenue, Changchun, Jilin, 130021, China. professorchen@foxmail.com.
Abstract
BACKGROUND: Our current understanding of the role of dequalinium chloride (DECA) in the progression of glioma remains very limited. This study was aimed to investigate the effect of DECA on human glioma cell lines in vitro and vivo. METHODS: The underlying molecular mechanism was analyzed for developing potential targeted agents. MTT assay, genomic DNA electrophoresis, DAPI staining, TUNEL staining, and wound scratch assay were performed to evaluate the effect of DECA on human glioma cell lines. Bioinformatics methods were used to screen the possible signaling pathway proteins, and the expression of these proteins and the corresponding mRNA was measured. RESULTS: DECA significantly inhibited the growth and proliferation of human glioma cells. Screening of apoptosis-related proteins showed the mRNA expression level of 6 genes was significantly changed after DECA administration. CONCLUSION: This study shows that DECA effectively inhibits the growth of glioma cells in vitro and vivo. DECA may promote glioma cell apoptosis by affecting the expression of NFKB2, HRAS, NF1, CBL, RAF1, and BCL-2 genes.
BACKGROUND: Our current understanding of the role of dequalinium chloride (DECA) in the progression of glioma remains very limited. This study was aimed to investigate the effect of DECA on humanglioma cell lines in vitro and vivo. METHODS: The underlying molecular mechanism was analyzed for developing potential targeted agents. MTT assay, genomic DNA electrophoresis, DAPI staining, TUNEL staining, and wound scratch assay were performed to evaluate the effect of DECA on humanglioma cell lines. Bioinformatics methods were used to screen the possible signaling pathway proteins, and the expression of these proteins and the corresponding mRNA was measured. RESULTS:DECA significantly inhibited the growth and proliferation of humanglioma cells. Screening of apoptosis-related proteins showed the mRNA expression level of 6 genes was significantly changed after DECA administration. CONCLUSION: This study shows that DECA effectively inhibits the growth of glioma cells in vitro and vivo. DECA may promote glioma cell apoptosis by affecting the expression of NFKB2, HRAS, NF1, CBL, RAF1, and BCL-2 genes.