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10.1371/journal.pone.0140782 http://scihub22266oqcxt.onion/10.1371/journal.pone.0140782 C4608773!4608773 !26474061     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26474061 &cmd=llinks): Failed to open stream: HTTP request failed! 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Elisidepsin Interacts Directly with Glycosylceramides in the Plasma Membrane of Tumor Cells to Induce Necrotic Cell Death |pdf=|usr=}}{{26474061 }} gab.com Text Elisidepsin Interacts Directly with Glycosylceramides in the Plasma Membrane of Tumor Cells to Induce Necrotic Cell Death JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26474061 #FOAvip Plasma membrane integrity is essential for cell life. Any major break on it immediately induces the death of the affected cell. Different molecules were described as disrupting this cell structure and thus showing antitumor activity. We have previously defined that elisidepsin (Irvalec®, PM02734) inserts and self-organizes in the plasma membrane of tumor cells, inducing a rapid loss of membrane integrity, cell permeabilization and necrotic death. Here we show that, in sensitive HCT-116 colorectal cells, all these effects are consequence of the interaction of elisidepsin with glycosylceramides in the cell membrane. Of note, an elisidepsin-resistant subline (HCT-116-Irv) presented reduced levels of glycosylceramides and no accumulation of elisidepsin in the plasma membrane. Consequently, drug treatment did not induce the characteristic necrotic cell death. Furthermore, GM95, a mutant derivative from B16 mouse melanoma cells lacking ceramide glucosyltransferase (UGCG) activity and thus the synthesis of glycosylceramides, was also resistant to elisidepsin. Over-expression of UGCG gene in these deficient cells restored glycosylceramides synthesis, rendering them sensitive to elisidepsin, at a similar level than parental B16 cells. These results indicate that glycosylceramides act as membrane targets of elisidepsin, facilitating its insertion in the plasma membrane and the subsequent membrane permeabilization that leads to drug-induced cell death. They also indicate that cell membrane lipids are a plausible target for antineoplastic therapy. Twit Text FOAVip Elisidepsin Interacts Directly with Glycosylceramides in the Plasma Membrane of Tumor Cells to Induce Necrotic Cell Death ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26474061 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26474061 #FOAvip English Wikipedia <ref>{{Cite pmid|26474061 }}</ref> Elisidepsin Interacts Directly with Glycosylceramides in the Plasma Membrane of Tumor Cells to Induce Necrotic Cell Death #MMPMID26474061 Molina-Guijarro JM ; García C ; Macías Á ; García-Fernández LF ; Moreno C ; Reyes F ; Martínez-Leal JF ; Fernández R ; Martínez V ; Valenzuela C ; Lillo MP ; Galmarini CM PLoS One 2015[]; 10 (10 ): e0140782 PMID26474061 show ga Plasma membrane integrity is essential for cell life. Any major break on it immediately induces the death of the affected cell. Different molecules were described as disrupting this cell structure and thus showing antitumor activity. We have previously defined that elisidepsin (Irvalec®, PM02734) inserts and self-organizes in the plasma membrane of tumor cells, inducing a rapid loss of membrane integrity, cell permeabilization and necrotic death. Here we show that, in sensitive HCT-116 colorectal cells, all these effects are consequence of the interaction of elisidepsin with glycosylceramides in the cell membrane. Of note, an elisidepsin-resistant subline (HCT-116-Irv) presented reduced levels of glycosylceramides and no accumulation of elisidepsin in the plasma membrane. Consequently, drug treatment did not induce the characteristic necrotic cell death. Furthermore, GM95, a mutant derivative from B16 mouse melanoma cells lacking ceramide glucosyltransferase (UGCG) activity and thus the synthesis of glycosylceramides, was also resistant to elisidepsin. Over-expression of UGCG gene in these deficient cells restored glycosylceramides synthesis, rendering them sensitive to elisidepsin, at a similar level than parental B16 cells. These results indicate that glycosylceramides act as membrane targets of elisidepsin, facilitating its insertion in the plasma membrane and the subsequent membrane permeabilization that leads to drug-induced cell death. They also indicate that cell membrane lipids are a plausible target for antineoplastic therapy. |Animals [MESH] |Cell Line, Tumor [MESH] |Cell Membrane/*metabolism/pathology [MESH] |Colorectal Neoplasms/drug therapy/genetics/*metabolism/pathology [MESH] |Depsipeptides/*pharmacology [MESH] |Glucosylceramides/genetics/*metabolism [MESH] |Humans [MESH] |Melanoma/drug therapy/genetics/*metabolism/pathology [MESH] |Mice [MESH]Elisidepsin Interacts Directly with Glycosylceramides in the Plasma Me(epmc).pdf DeepDyve Pubget Overpricing