Publication: Cysteinyl leukotriene receptor antagonists induce apoptosis and inhibit proliferation of human glioblastoma cells by downregulating b-cell lymphoma 2 and inducing cell cycle arrest
Issued Date
2018-01-01
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ISSN
12057541
00084212
00084212
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2-s2.0-85050941403
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Mahidol University
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SCOPUS
Bibliographic Citation
Canadian Journal of Physiology and Pharmacology. Vol.96, No.8 (2018), 798-806
Suggested Citation
Pannaree Piromkraipak, Tipparat Parakaw, Suttinee Phuagkhaopong, Sirada Srihirun, Sukumal Chongthammakun, Kulathida Chaithirayanon, Pornpun Vivithanaporn Cysteinyl leukotriene receptor antagonists induce apoptosis and inhibit proliferation of human glioblastoma cells by downregulating b-cell lymphoma 2 and inducing cell cycle arrest. Canadian Journal of Physiology and Pharmacology. Vol.96, No.8 (2018), 798-806. doi:10.1139/cjpp-2017-0757 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/45277
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Title
Cysteinyl leukotriene receptor antagonists induce apoptosis and inhibit proliferation of human glioblastoma cells by downregulating b-cell lymphoma 2 and inducing cell cycle arrest
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Abstract
© 2018, Canadian Science Publishing. All rights reserved. Glioblastoma is the most aggressive type of brain cancer with the highest proliferation, invasion, and migration. Montelukast and zafirlukast, 2 widely used leukotriene receptor antagonists (LTRAs) for asthma treatment, inhibited invasion and migration of glioblastoma cell lines. Montelukast induces apoptosis and inhibits cell proliferation of various cancer cells. Herein, apoptotic and antiproliferative effects of montelukast and zafirlukast were investigated in 2 glioblastoma cell lines, A172 and U-87 MG. Both LTRAs induced apoptosis and inhibited cell proliferation of glioblastoma cells in a concentration-dependent manner. Montelukast was more cytotoxic and induced higher levels of apoptosis than zafirlukast in A172 cells, but not in U-87 MG cells. Both drugs decreased expression of B-cell lymphoma 2 (Bcl-2) protein without affecting Bcl-2-associated X (Bax) levels. LTRAs also reduced the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). In contrast, zafirlukast showed a greater antiproliferative effect than montelukast and induced G0/G1 cell cycle arrest by upregulating p53 and p21 expression. These results suggested the therapeutic potential of LTRAs in glioblastoma.