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Forside

Cancer cells become susceptible to natural killer cell killing after exposure to histone deacetylase inhibitors due to glycogen synthase kinase-3-dependent expression of MHC class I-related chain A and B

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Cancer cells become susceptible to natural killer cell killing after exposure to histone deacetylase inhibitors due to glycogen synthase kinase-3-dependent expression of MHC class I-related chain A and B. / Skov, Søren; Pedersen, Marianne Terndrup; Andresen, Lars; Straten, Per Thor; Woetmann, Anders; Odum, Niels.

I: Cancer Research, Bind 65, Nr. 23, 2005, s. 11136-45.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Skov, S, Pedersen, MT, Andresen, L, Straten, PT, Woetmann, A & Odum, N 2005, 'Cancer cells become susceptible to natural killer cell killing after exposure to histone deacetylase inhibitors due to glycogen synthase kinase-3-dependent expression of MHC class I-related chain A and B', Cancer Research, bind 65, nr. 23, s. 11136-45. https://doi.org/10.1158/0008-5472.CAN-05-0599

APA

Skov, S., Pedersen, M. T., Andresen, L., Straten, P. T., Woetmann, A., & Odum, N. (2005). Cancer cells become susceptible to natural killer cell killing after exposure to histone deacetylase inhibitors due to glycogen synthase kinase-3-dependent expression of MHC class I-related chain A and B. Cancer Research, 65(23), 11136-45. https://doi.org/10.1158/0008-5472.CAN-05-0599

Vancouver

Skov S, Pedersen MT, Andresen L, Straten PT, Woetmann A, Odum N. Cancer cells become susceptible to natural killer cell killing after exposure to histone deacetylase inhibitors due to glycogen synthase kinase-3-dependent expression of MHC class I-related chain A and B. Cancer Research. 2005;65(23):11136-45. https://doi.org/10.1158/0008-5472.CAN-05-0599

Author

Skov, Søren ; Pedersen, Marianne Terndrup ; Andresen, Lars ; Straten, Per Thor ; Woetmann, Anders ; Odum, Niels. / Cancer cells become susceptible to natural killer cell killing after exposure to histone deacetylase inhibitors due to glycogen synthase kinase-3-dependent expression of MHC class I-related chain A and B. I: Cancer Research. 2005 ; Bind 65, Nr. 23. s. 11136-45.

Bibtex

@article{1b9c94a0fcf011ddb219000ea68e967b,
title = "Cancer cells become susceptible to natural killer cell killing after exposure to histone deacetylase inhibitors due to glycogen synthase kinase-3-dependent expression of MHC class I-related chain A and B",
abstract = "We show that histone deacetylase (HDAC) inhibitors lead to functional expression of MHC class I-related chain A and B (MICA/B) on cancer cells, making them potent targets for natural killer (NK) cell-mediated killing through a NK group 2, member D (NKG2D) restricted mechanism. Blocking either apoptosis or oxidative stress caused by HDAC inhibitor treatment did not affect MICA/B expression, suggesting involvement of a separate signal pathway not directly coupled to induction of cell death. HDAC inhibitor treatment induced glycogen synthase kinase-3 (GSK-3) activity and down-regulation of GSK-3 by small interfering RNA or by different inhibitors showed that GSK-3 activity is essential for the induced MICA/B expression. We thus present evidence that cancer cells which survive the direct induction of cell death by HDAC inhibitors become targets for NKG2D-expressing cells like NK cells, gammadelta T cells, and CD8 T cells.",
author = "S{\o}ren Skov and Pedersen, {Marianne Terndrup} and Lars Andresen and Straten, {Per Thor} and Anders Woetmann and Niels Odum",
note = "Keywords: Antibiotics, Antineoplastic; Apoptosis; Cell Line, Tumor; Depsipeptides; Enzyme Inhibitors; Glycogen Synthase Kinase 3; Histocompatibility Antigens Class I; Histone Deacetylases; Humans; Jurkat Cells; Killer Cells, Natural; Neoplasms; T-Lymphocytes",
year = "2005",
doi = "10.1158/0008-5472.CAN-05-0599",
language = "English",
volume = "65",
pages = "11136--45",
journal = "Cancer Research",
issn = "0008-5472",
publisher = "American Association for Cancer Research",
number = "23",

}

RIS

TY - JOUR

T1 - Cancer cells become susceptible to natural killer cell killing after exposure to histone deacetylase inhibitors due to glycogen synthase kinase-3-dependent expression of MHC class I-related chain A and B

AU - Skov, Søren

AU - Pedersen, Marianne Terndrup

AU - Andresen, Lars

AU - Straten, Per Thor

AU - Woetmann, Anders

AU - Odum, Niels

N1 - Keywords: Antibiotics, Antineoplastic; Apoptosis; Cell Line, Tumor; Depsipeptides; Enzyme Inhibitors; Glycogen Synthase Kinase 3; Histocompatibility Antigens Class I; Histone Deacetylases; Humans; Jurkat Cells; Killer Cells, Natural; Neoplasms; T-Lymphocytes

PY - 2005

Y1 - 2005

N2 - We show that histone deacetylase (HDAC) inhibitors lead to functional expression of MHC class I-related chain A and B (MICA/B) on cancer cells, making them potent targets for natural killer (NK) cell-mediated killing through a NK group 2, member D (NKG2D) restricted mechanism. Blocking either apoptosis or oxidative stress caused by HDAC inhibitor treatment did not affect MICA/B expression, suggesting involvement of a separate signal pathway not directly coupled to induction of cell death. HDAC inhibitor treatment induced glycogen synthase kinase-3 (GSK-3) activity and down-regulation of GSK-3 by small interfering RNA or by different inhibitors showed that GSK-3 activity is essential for the induced MICA/B expression. We thus present evidence that cancer cells which survive the direct induction of cell death by HDAC inhibitors become targets for NKG2D-expressing cells like NK cells, gammadelta T cells, and CD8 T cells.

AB - We show that histone deacetylase (HDAC) inhibitors lead to functional expression of MHC class I-related chain A and B (MICA/B) on cancer cells, making them potent targets for natural killer (NK) cell-mediated killing through a NK group 2, member D (NKG2D) restricted mechanism. Blocking either apoptosis or oxidative stress caused by HDAC inhibitor treatment did not affect MICA/B expression, suggesting involvement of a separate signal pathway not directly coupled to induction of cell death. HDAC inhibitor treatment induced glycogen synthase kinase-3 (GSK-3) activity and down-regulation of GSK-3 by small interfering RNA or by different inhibitors showed that GSK-3 activity is essential for the induced MICA/B expression. We thus present evidence that cancer cells which survive the direct induction of cell death by HDAC inhibitors become targets for NKG2D-expressing cells like NK cells, gammadelta T cells, and CD8 T cells.

U2 - 10.1158/0008-5472.CAN-05-0599

DO - 10.1158/0008-5472.CAN-05-0599

M3 - Journal article

C2 - 16322264

VL - 65

SP - 11136

EP - 11145

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 23

ER -

ID: 10615235