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Novel glycolipid agents for killing cisplatin-resistant human epithelial ovarian cancer cells
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نویسنده
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moraya a.i. ,ali j.l. ,samadder p. ,liang l. ,morrison l.c. ,werbowetski-ogilvie t.e. ,ogunsina m. ,schweizer f. ,arthur g. ,nachtigal m.w.
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منبع
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journal of experimental and clinical cancer research - 2017 - دوره : 36 - شماره : 1
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چکیده
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Background: chemotherapy resistance is one of the major factors contributing to mortality from human epithelial ovarian cancer (eoc). identifying drugs that can effectively kill chemotherapy-resistant eoc cells would be a major advance in reducing mortality. glycosylated antitumour ether lipids (gaels) are synthetic glycolipids that are cytotoxic to a wide range of cancer cells. they appear to induce cancer cell death in an apoptosis-independent manner. methods: herein,the effectiveness of two gaels,gln and mo-101,in killing chemotherapy-sensitive and-resistant eoc cells lines and primary cell samples was tested using monolayer,non-adherent aggregate,and non-adherent spheroid cultures. results: our results show that eoc cells exhibit a differential sensitivity to the gaels. strikingly,both gaels are capable of inducing eoc cell death in chemotherapy-sensitive and-resistant cells grown as monolayer or non-adherent cultures. mechanistic studies provide evidence that apoptotic-cell death (caspase activation) contributes to,but is not completely responsible for,gael-induced cell killing in the a2780-cp eoc cell line,but not primary eoc cell samples. conclusions: studies using primary eoc cell samples supports previously published work showing a gael-induced caspase-independent mechanism of death. gaels hold promise for development as novel compounds to combat eoc mortality due to chemotherapy resistance. © 2017 the author(s).
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کلیدواژه
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Drug-resistance; Glycosylated anti-tumour ether lipid; Ovarian cancer; Spheroid
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آدرس
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dept. of biochemistry and medical genetics,university of manitoba,room 333 bmsb,745 bannatyne avenue,winnipeg,mb r3e 0 w9, Canada, dept. of biochemistry and medical genetics,university of manitoba,room 333 bmsb,745 bannatyne avenue,winnipeg,mb r3e 0 w9, Canada, dept. of biochemistry and medical genetics,university of manitoba,room 333 bmsb,745 bannatyne avenue,winnipeg,mb r3e 0 w9, Canada, dept. of biochemistry and medical genetics,university of manitoba,room 333 bmsb,745 bannatyne avenue,winnipeg,mb r3e 0 w9, Canada, dept. of biochemistry and medical genetics,university of manitoba,room 333 bmsb,745 bannatyne avenue,winnipeg,mb r3e 0 w9, Canada, dept. of biochemistry and medical genetics,university of manitoba,room 333 bmsb,745 bannatyne avenue,winnipeg,mb r3e 0 w9, Canada, dept. of chemistry,university of manitoba,winnipeg, Canada, dept. of chemistry,university of manitoba,winnipeg, Canada, dept. of biochemistry and medical genetics,university of manitoba,room 333 bmsb,745 bannatyne avenue,winnipeg,mb r3e 0 w9, Canada, dept. of biochemistry and medical genetics,university of manitoba,room 333 bmsb,745 bannatyne avenue,winnipeg,mb r3e 0 w9,canada,dept. of obstetrics,gynecology and reproductive sciences,university of manitoba,winnipeg,canada,research institute in oncology and hematology,cancercare manitoba,winnipeg,canada,manitoba ovarian cancer outcome (moco) study group,winnipeg, Canada
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Authors
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