دورية أكاديمية

Caspase-8 deficiency induces a switch from TLR3 induced apoptosis to lysosomal cell death in neuroblastoma.

التفاصيل البيبلوغرافية
العنوان: Caspase-8 deficiency induces a switch from TLR3 induced apoptosis to lysosomal cell death in neuroblastoma.
المؤلفون: Locquet MA; Childhood Cancers and Cell Death Laboratory, Cancer Research Center of Lyon (CRCL), INSERM 1052, CNRS 5286, Lyon, France., Ichim G; Cancer Cell Death Laboratory, Part of LabEx DEVweCAN, Cancer Initiation and Tumoral Cell Identity Department, CRCL, Lyon, France., Bisaccia J; Childhood Cancers and Cell Death Laboratory, Cancer Research Center of Lyon (CRCL), INSERM 1052, CNRS 5286, Lyon, France., Dutour A; Childhood Cancers and Cell Death Laboratory, Cancer Research Center of Lyon (CRCL), INSERM 1052, CNRS 5286, Lyon, France., Lebecque S; Childhood Cancers and Cell Death Laboratory, Cancer Research Center of Lyon (CRCL), INSERM 1052, CNRS 5286, Lyon, France.; Service D'Anatomie Pathologique, Hospices Civils de Lyon, Hôpital Lyon Sud, Pierre-Bénite, France., Castets M; Childhood Cancers and Cell Death Laboratory, Cancer Research Center of Lyon (CRCL), INSERM 1052, CNRS 5286, Lyon, France. marie.castets@lyon.unicancer.fr., Weber K; Childhood Cancers and Cell Death Laboratory, Cancer Research Center of Lyon (CRCL), INSERM 1052, CNRS 5286, Lyon, France. katrin.weber@lyon.unicancer.fr.
المصدر: Scientific reports [Sci Rep] 2021 May 19; Vol. 11 (1), pp. 10609. Date of Electronic Publication: 2021 May 19.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101563288 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-2322 (Electronic) Linking ISSN: 20452322 NLM ISO Abbreviation: Sci Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : Nature Publishing Group, copyright 2011-
مواضيع طبية MeSH: Apoptosis*/drug effects, Caspase 8/*metabolism , Neuroblastoma/*metabolism , Neuroblastoma/*pathology , Toll-Like Receptor 3/*metabolism, Cell Line, Tumor ; Enzyme Activation/drug effects ; Humans ; Interferon Type I/pharmacology ; Intracellular Membranes/drug effects ; Intracellular Membranes/metabolism ; Lysosomes/drug effects ; Lysosomes/metabolism ; Necroptosis/drug effects ; Permeability/drug effects ; Poly I-C/pharmacology
مستخلص: In cancer cells only, TLR3 acquires death receptor properties by efficiently triggering the extrinsic pathway of apoptosis with Caspase-8 as apical protease. Here, we demonstrate that in the absence of Caspase-8, activation of TLR3 can trigger a form of programmed cell death, which is distinct from classical apoptosis. When TLR3 was activated in the Caspase-8 negative neuroblastoma cell line SH-SY5Y, cell death was accompanied by lysosomal permeabilization. Despite caspases being activated, lysosomal permeabilization as well as cell death were not affected by blocking caspase-activity, positioning lysosomal membrane permeabilization (LMP) upstream of caspase activation. Taken together, our data suggest that LMP with its deadly consequences represents a "default" death mechanism in cancer cells, when Caspase-8 is absent and apoptosis cannot be induced.
References: Cell Death Differ. 2017 Jul;24(7):1184-1195. (PMID: 28498367)
J Immunol. 2006 Apr 15;176(8):4894-901. (PMID: 16585585)
Cancer Res. 2000 Aug 15;60(16):4315-9. (PMID: 10969767)
Cancer Lett. 2020 Mar 1;472:29-39. (PMID: 31838086)
J Biol Chem. 2001 Feb 2;276(5):3149-57. (PMID: 11073962)
Cell Death Differ. 2012 Sep;19(9):1482-94. (PMID: 22421964)
Front Mol Neurosci. 2019 Jan 29;12:9. (PMID: 30760980)
J Cell Biol. 2001 May 28;153(5):999-1010. (PMID: 11381085)
Trends Biochem Sci. 2019 Jan;44(1):53-63. (PMID: 30509860)
Mol Cell. 2011 Aug 5;43(3):449-63. (PMID: 21737330)
IUBMB Life. 2005 Apr-May;57(4-5):347-53. (PMID: 16036619)
Nature. 2006 May 4;441(7089):101-5. (PMID: 16625202)
J Clin Invest. 2000 Nov;106(9):1127-37. (PMID: 11067865)
Eur J Pharmacol. 2005 Nov 7;524(1-3):49-52. (PMID: 16243312)
Cell. 2011 Mar 4;144(5):646-74. (PMID: 21376230)
Med Pediatr Oncol. 2000 Dec;35(6):603-7. (PMID: 11107127)
J Biol Chem. 2004 Jan 30;279(5):3578-87. (PMID: 14581476)
Cell Death Dis. 2018 Aug 29;9(9):874. (PMID: 30158588)
J Hepatol. 2019 Oct;71(4):763-772. (PMID: 31220470)
Cancer Res. 2007 Mar 1;67(5):2217-25. (PMID: 17332352)
Nat Immunol. 2010 May;11(5):373-84. (PMID: 20404851)
Nature. 2001 Oct 18;413(6857):732-8. (PMID: 11607032)
Biochim Biophys Acta. 2011 Apr;1813(4):521-31. (PMID: 21195116)
J Exp Med. 2011 Sep 26;208(10):2083-98. (PMID: 21911422)
J Immunol. 2013 Jan 15;190(2):764-73. (PMID: 23255358)
J Biomed Sci. 2011 Aug 23;18:65. (PMID: 21861882)
Am J Physiol Gastrointest Liver Physiol. 2002 Oct;283(4):G947-56. (PMID: 12223355)
Oncogene. 2006 Aug 24;25(37):5125-33. (PMID: 16607283)
Cell Death Differ. 2000 Dec;7(12):1166-73. (PMID: 11175253)
Traffic. 2018 Dec;19(12):918-931. (PMID: 30125440)
Neuroreport. 2007 Oct 29;18(16):1725-8. (PMID: 17921876)
Nat Rev Cancer. 2005 Nov;5(11):886-97. (PMID: 16239905)
Blood. 2011 Apr 28;117(17):4519-29. (PMID: 21378274)
Front Immunol. 2017 Dec 21;8:1897. (PMID: 29312355)
Nat Rev Mol Cell Biol. 2010 Oct;11(10):700-14. (PMID: 20823910)
المشرفين على المادة: 0 (Interferon Type I)
0 (Toll-Like Receptor 3)
EC 3.4.22.- (Caspase 8)
O84C90HH2L (Poly I-C)
تواريخ الأحداث: Date Created: 20210520 Date Completed: 20211028 Latest Revision: 20211028
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC8134575
DOI: 10.1038/s41598-021-89793-1
PMID: 34011952
قاعدة البيانات: MEDLINE
الوصف
تدمد:2045-2322
DOI:10.1038/s41598-021-89793-1