SLFN11 Inactivation Induces Proteotoxic Stress and Sensitizes Cancer Cells to Ubiquitin Activating Enzyme Inhibitor TAK-243.

Apoptosis Biomarkers, Tumor / genetics Cell Proliferation Drug Resistance, Neoplasm Endoplasmic Reticulum Stress Gene Expression Regulation, Neoplastic Humans Neoplasms / drug therapy Nuclear Proteins / antagonists & inhibitors Phosphorylation Pyrazoles / pharmacology Pyrimidines / pharmacology Sulfides / pharmacology Sulfonamides / pharmacology Tumor Cells, Cultured Ubiquitin-Activating Enzymes / antagonists & inhibitors Ubiquitination

Journal

Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R

Informations de publication

Date de publication:
01 06 2021
Historique:
received: 13 08 2020
revised: 10 12 2020
accepted: 13 04 2021
pubmed: 18 4 2021
medline: 5 11 2021
entrez: 17 4 2021
Statut: ppublish

Résumé

Schlafen11 (SLFN11) inactivation occurs in approximately 50% of cancer cell lines and in a large fraction of patient tumor samples, which leads to chemoresistance. Therefore, new therapeutic approaches are needed to target

Identifiants

DOI: 10.1158/0008-5472.CAN-20-2694 PMID: 33863777 PMC: PMC8178208
pubmed: 33863777
pii: 0008-5472.CAN-20-2694
doi: 10.1158/0008-5472.CAN-20-2694
pmc: PMC8178208
mid: NIHMS1696339
doi:

Substances chimiques

Biomarkers, Tumor 0
Nuclear Proteins 0
Pyrazoles 0
Pyrimidines 0
SLFN11 protein, human 0
Sulfides 0
Sulfonamides 0
Ubiquitin-Activating Enzymes EC 6.2.1.45
TAK-243 V9GGV0YCDI

Types de publication

Journal Article Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

3067-3078

Subventions

Organisme : Intramural NIH HHS
ID : Z01 BC006150
Pays : United States

Informations de copyright

©2021 American Association for Cancer Research.

Références

Cancers (Basel). 2021 Feb 10;13(4):
pubmed: 33578789
Nature. 2007 Jun 28;447(7148):1135-8
pubmed: 17597759
Proc Natl Acad Sci U S A. 2012 Sep 11;109(37):15030-5
pubmed: 22927417
Mol Cell Biol. 2007 Aug;27(16):5806-18
pubmed: 17515603
Int Rev Cell Mol Biol. 2011;292:197-280
pubmed: 22078962
Nat Rev Cancer. 2014 Sep;14(9):581-97
pubmed: 25145482
Pharmacol Ther. 2019 Sep;201:94-102
pubmed: 31128155
Oncotarget. 2018 Apr 17;9(29):20265-20281
pubmed: 29755650
Blood Adv. 2019 Jan 8;3(1):51-62
pubmed: 30617217
Biochem J. 2008 Jul 15;413(2):239-50
pubmed: 18373498
Oncotarget. 2016 Jun 28;7(26):39396-39407
pubmed: 27276683
Nat Rev Neurol. 2017 Aug;13(8):477-491
pubmed: 28731040
Nat Rev Cancer. 2008 Dec;8(12):957-67
pubmed: 19005492
J Virol. 2019 Jul 17;93(15):
pubmed: 31118262
Nature. 2012 Mar 28;483(7391):603-7
pubmed: 22460905
Mol Cell. 2006 Sep 15;23(6):887-97
pubmed: 16973440
Oncogene. 2017 Feb 2;36(5):678-686
pubmed: 27375025
Nat Struct Mol Biol. 2018 Nov;25(11):1047-1058
pubmed: 30374083
Cell Rep. 2020 Mar 24;30(12):4137-4151.e6
pubmed: 32209474
Virchows Arch. 2021 Mar;478(3):567-568
pubmed: 33566168
Oncotarget. 2016 Nov 22;7(47):76534-76550
pubmed: 27708213
Mol Biol Cell. 2016 Apr 15;27(8):1188-96
pubmed: 26912792
Nat Cell Biol. 2011 Mar;13(3):184-90
pubmed: 21364565
Leuk Lymphoma. 2019 Dec;60(12):2946-2950
pubmed: 31111763
Proc Natl Acad Sci U S A. 2021 Feb 9;118(6):
pubmed: 33536335
Nat Commun. 2018 Mar 21;9(1):1165
pubmed: 29563550
J Cell Sci. 2010 Sep 1;123(Pt 17):2892-900
pubmed: 20682638
BMC Cancer. 2020 Nov 20;20(1):1123
pubmed: 33218331
PLoS One. 2021 Jan 29;16(1):e0237554
pubmed: 33513156
Nat Rev Mol Cell Biol. 2017 Oct;18(10):622-636
pubmed: 28811666
Leukemia. 2019 Jan;33(1):37-51
pubmed: 29884901
FEBS J. 2019 Feb;286(3):441-455
pubmed: 29931808
Blood. 2021 Jan 21;137(3):336-348
pubmed: 32735670
J Biol Chem. 2013 Mar 15;288(11):7606-7617
pubmed: 23341460
PLoS Pathog. 2016 Dec 27;12(12):e1006066
pubmed: 28027315
Open Biol. 2018 Sep 26;8(9):
pubmed: 30257893
Virchows Arch. 2021 Mar;478(3):569-579
pubmed: 32474729
Br J Cancer. 2021 Mar;124(5):951-962
pubmed: 33339894
Nat Immunol. 2010 Apr;11(4):335-43
pubmed: 20190759
Cell Mol Life Sci. 2014 Jun;71(12):2289-97
pubmed: 24448903
Science. 2011 Nov 25;334(6059):1081-6
pubmed: 22116877
J Med Chem. 2015 Dec 24;58(24):9480-97
pubmed: 26565666
Mol Cell. 2018 Feb 1;69(3):371-384.e6
pubmed: 29395061
Nat Med. 2018 Feb;24(2):186-193
pubmed: 29334375
Blood. 2019 Apr 4;133(14):1572-1584
pubmed: 30737236
Nature. 2012 Nov 1;491(7422):125-8
pubmed: 23000900
EMBO Rep. 2016 Jan;17(1):94-109
pubmed: 26658330
Nat Struct Mol Biol. 2014 Apr;21(4):325-35
pubmed: 24699081
Theranostics. 2020 Mar 25;10(10):4627-4643
pubmed: 32292519
Oncotarget. 2018 Sep 28;9(76):34198-34199
pubmed: 30344936

Auteurs

Yasuhisa Murai (Y)

Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Department of Gastroenterology and Hematology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
ORCID: 0000-0002-3305-1248

Ukhyun Jo (U)

Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
ORCID: 0000-0002-2826-1355

Junko Murai (J)

Institute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata, Japan.

Lisa M Jenkins (LM)

Laboratory of Cell Biology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
ORCID: 0000-0003-1245-1338

Shar-Yin N Huang (SN)

Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Sirisha Chakka (S)

National Center for Advancing Translational Sciences, Functional Genomics Laboratory, NIH, Rockville, Maryland.

Lu Chen (L)

National Center for Advancing Translational Sciences, Functional Genomics Laboratory, NIH, Rockville, Maryland.

Ken Cheng (K)

National Center for Advancing Translational Sciences, Functional Genomics Laboratory, NIH, Rockville, Maryland.

Shinsaku Fukuda (S)

Department of Gastroenterology and Hematology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Naoko Takebe (N)

Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Division of Cancer Treatment and Diagnosis, NCI, NIH, Bethesda, Maryland.
ORCID: 0000-0002-5790-4954

Yves Pommier (Y)

Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland. pommier@nih.gov.

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Classifications MeSH

questionsmedicales.fr › Phénomènes physiologiques cellulaires › Mort cellulaire › Mort cellulaire régulée › Apoptose › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Facteurs biologiques › Marqueurs biologiques › Marqueurs biologiques tumoraux › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Phénomènes physiologiques › Croissance et développement › Croissance › Processus de croissance cellulaire › Prolifération cellulaire › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Phénomènes physiologiques › Phénomènes pharmacologiques et toxicologiques › Phénomènes pharmacologiques › Résistance aux substances › Résistance aux médicaments antinéoplasiques › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Stress du réticulum endoplasmique › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Phénomènes génétiques › Régulation de l'expression des gènes › Régulation de l'expression des gènes tumoraux › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Tumeurs › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines nucléaires › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Métabolisme › Phosphorylation › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Composés hétérocycliques › Composés hétéromonocycliques › Azoles › Pyrazoles › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Composés hétérocycliques › Composés hétéromonocycliques › Pyrimidines › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Composés chimiques organiques › Composés du soufre › Sulfures › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Composés chimiques organiques › Composés du soufre › Sulfones › Sulfonamides › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Cellules › Cellules cultivées › Cellules cancéreuses en culture › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Enzymes et coenzymes › Enzymes › Ligases › Ubiquitin-protein ligase complexes › Ubiquitin-activating enzymes › SLFN11 Inactivation Induces Proteotoxic Stress...
questionsmedicales.fr › Phénomènes génétiques › Régulation de l'expression des gènes › Modification traductionnelle des protéines › Maturation post-traductionnelle des protéines › Ubiquitination › SLFN11 Inactivation Induces Proteotoxic Stress...