Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase

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Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase. / Petersen, Nikolaj H T; Olsen, Ole D; Groth-Pedersen, Line; Ellegaard, Anne-Marie; Bilgin, Mesut; Redmer, Susanne; Ostenfeld, Marie Stampe; Ulanet, Danielle; Dovmark, Tobias H; Lønborg, Andreas; Vindeløv, Signe D; Hanahan, Douglas; Arenz, Christoph; Ejsing, Christer S; Kirkegaard, Thomas; Rohde, Mikkel; Nylandsted, Jesper; Jäättelä, Marja.

I: Cancer Cell, Bind 24, Nr. 3, 09.09.2013, s. 379-93.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Petersen, NHT, Olsen, OD, Groth-Pedersen, L, Ellegaard, A-M, Bilgin, M, Redmer, S, Ostenfeld, MS, Ulanet, D, Dovmark, TH, Lønborg, A, Vindeløv, SD, Hanahan, D, Arenz, C, Ejsing, CS, Kirkegaard, T, Rohde, M, Nylandsted, J & Jäättelä, M 2013, 'Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase', Cancer Cell, bind 24, nr. 3, s. 379-93. https://doi.org/10.1016/j.ccr.2013.08.003

APA

Petersen, N. H. T., Olsen, O. D., Groth-Pedersen, L., Ellegaard, A-M., Bilgin, M., Redmer, S., Ostenfeld, M. S., Ulanet, D., Dovmark, T. H., Lønborg, A., Vindeløv, S. D., Hanahan, D., Arenz, C., Ejsing, C. S., Kirkegaard, T., Rohde, M., Nylandsted, J., & Jäättelä, M. (2013). Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase. Cancer Cell, 24(3), 379-93. https://doi.org/10.1016/j.ccr.2013.08.003

CBE

Petersen NHT, Olsen OD, Groth-Pedersen L, Ellegaard A-M, Bilgin M, Redmer S, Ostenfeld MS, Ulanet D, Dovmark TH, Lønborg A, Vindeløv SD, Hanahan D, Arenz C, Ejsing CS, Kirkegaard T, Rohde M, Nylandsted J, Jäättelä M. 2013. Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase. Cancer Cell. 24(3):379-93. https://doi.org/10.1016/j.ccr.2013.08.003

MLA

Vancouver

Author

Petersen, Nikolaj H T ; Olsen, Ole D ; Groth-Pedersen, Line ; Ellegaard, Anne-Marie ; Bilgin, Mesut ; Redmer, Susanne ; Ostenfeld, Marie Stampe ; Ulanet, Danielle ; Dovmark, Tobias H ; Lønborg, Andreas ; Vindeløv, Signe D ; Hanahan, Douglas ; Arenz, Christoph ; Ejsing, Christer S ; Kirkegaard, Thomas ; Rohde, Mikkel ; Nylandsted, Jesper ; Jäättelä, Marja. / Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase. I: Cancer Cell. 2013 ; Bind 24, Nr. 3. s. 379-93.

Bibtex

@article{981f0e5e291849daa117b94e14296363,
title = "Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase",
abstract = "Lysosomal membrane permeabilization and subsequent cell death may prove useful in cancer treatment, provided that cancer cell lysosomes can be specifically targeted. Here, we identify acid sphingomyelinase (ASM) inhibition as a selective means to destabilize cancer cell lysosomes. Lysosome-destabilizing experimental anticancer agent siramesine inhibits ASM by interfering with the binding of ASM to its essential lysosomal cofactor, bis(monoacylglycero)phosphate. Like siramesine, several clinically relevant ASM inhibitors trigger cancer-specific lysosomal cell death, reduce tumor growth in vivo, and revert multidrug resistance. Their cancer selectivity is associated with transformation-associated reduction in ASM expression and subsequent failure to maintain sphingomyelin hydrolysis during drug exposure. Taken together, these data identify ASM as an attractive target for cancer therapy.",
keywords = "Animals, Antineoplastic Agents, Cell Death, Cell Line, Tumor, Cell Transformation, Neoplastic, Drug Resistance, Neoplasm, Enzyme Activation, Enzyme Inhibitors, Female, HSP70 Heat-Shock Proteins, Humans, Indoles, Lysosomes, Mice, Mice, Transgenic, Phenotype, Sphingolipids, Sphingomyelin Phosphodiesterase, Spiro Compounds, Tocopherols, Xenograft Model Antitumor Assays",
author = "Petersen, {Nikolaj H T} and Olsen, {Ole D} and Line Groth-Pedersen and Anne-Marie Ellegaard and Mesut Bilgin and Susanne Redmer and Ostenfeld, {Marie Stampe} and Danielle Ulanet and Dovmark, {Tobias H} and Andreas L{\o}nborg and Vindel{\o}v, {Signe D} and Douglas Hanahan and Christoph Arenz and Ejsing, {Christer S} and Thomas Kirkegaard and Mikkel Rohde and Jesper Nylandsted and Marja J{\"a}{\"a}ttel{\"a}",
note = "Copyright {\textcopyright} 2013 Elsevier Inc. All rights reserved.",
year = "2013",
month = sep,
day = "9",
doi = "10.1016/j.ccr.2013.08.003",
language = "English",
volume = "24",
pages = "379--93",
journal = "Cancer Cell",
issn = "1535-6108",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase

AU - Petersen, Nikolaj H T

AU - Olsen, Ole D

AU - Groth-Pedersen, Line

AU - Ellegaard, Anne-Marie

AU - Bilgin, Mesut

AU - Redmer, Susanne

AU - Ostenfeld, Marie Stampe

AU - Ulanet, Danielle

AU - Dovmark, Tobias H

AU - Lønborg, Andreas

AU - Vindeløv, Signe D

AU - Hanahan, Douglas

AU - Arenz, Christoph

AU - Ejsing, Christer S

AU - Kirkegaard, Thomas

AU - Rohde, Mikkel

AU - Nylandsted, Jesper

AU - Jäättelä, Marja

N1 - Copyright © 2013 Elsevier Inc. All rights reserved.

PY - 2013/9/9

Y1 - 2013/9/9

N2 - Lysosomal membrane permeabilization and subsequent cell death may prove useful in cancer treatment, provided that cancer cell lysosomes can be specifically targeted. Here, we identify acid sphingomyelinase (ASM) inhibition as a selective means to destabilize cancer cell lysosomes. Lysosome-destabilizing experimental anticancer agent siramesine inhibits ASM by interfering with the binding of ASM to its essential lysosomal cofactor, bis(monoacylglycero)phosphate. Like siramesine, several clinically relevant ASM inhibitors trigger cancer-specific lysosomal cell death, reduce tumor growth in vivo, and revert multidrug resistance. Their cancer selectivity is associated with transformation-associated reduction in ASM expression and subsequent failure to maintain sphingomyelin hydrolysis during drug exposure. Taken together, these data identify ASM as an attractive target for cancer therapy.

AB - Lysosomal membrane permeabilization and subsequent cell death may prove useful in cancer treatment, provided that cancer cell lysosomes can be specifically targeted. Here, we identify acid sphingomyelinase (ASM) inhibition as a selective means to destabilize cancer cell lysosomes. Lysosome-destabilizing experimental anticancer agent siramesine inhibits ASM by interfering with the binding of ASM to its essential lysosomal cofactor, bis(monoacylglycero)phosphate. Like siramesine, several clinically relevant ASM inhibitors trigger cancer-specific lysosomal cell death, reduce tumor growth in vivo, and revert multidrug resistance. Their cancer selectivity is associated with transformation-associated reduction in ASM expression and subsequent failure to maintain sphingomyelin hydrolysis during drug exposure. Taken together, these data identify ASM as an attractive target for cancer therapy.

KW - Animals

KW - Antineoplastic Agents

KW - Cell Death

KW - Cell Line, Tumor

KW - Cell Transformation, Neoplastic

KW - Drug Resistance, Neoplasm

KW - Enzyme Activation

KW - Enzyme Inhibitors

KW - Female

KW - HSP70 Heat-Shock Proteins

KW - Humans

KW - Indoles

KW - Lysosomes

KW - Mice

KW - Mice, Transgenic

KW - Phenotype

KW - Sphingolipids

KW - Sphingomyelin Phosphodiesterase

KW - Spiro Compounds

KW - Tocopherols

KW - Xenograft Model Antitumor Assays

U2 - 10.1016/j.ccr.2013.08.003

DO - 10.1016/j.ccr.2013.08.003

M3 - Journal article

C2 - 24029234

VL - 24

SP - 379

EP - 393

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 3

ER -