دورية أكاديمية

Death Receptors DR4 and DR5 Undergo Spontaneous and Ligand-Mediated Endocytosis and Recycling Regardless of the Sensitivity of Cancer Cells to TRAIL.

التفاصيل البيبلوغرافية
العنوان: Death Receptors DR4 and DR5 Undergo Spontaneous and Ligand-Mediated Endocytosis and Recycling Regardless of the Sensitivity of Cancer Cells to TRAIL.
المؤلفون: Artykov AA; Department of Bioengineering, Institute of Bioorganic Chemistry (RAS), Moscow, Russia., Yagolovich AV; Department of Bioengineering, Institute of Bioorganic Chemistry (RAS), Moscow, Russia.; Faculty of Biology, Lomonosov Moscow State University, Moscow, Russia., Dolgikh DA; Department of Bioengineering, Institute of Bioorganic Chemistry (RAS), Moscow, Russia.; Faculty of Biology, Lomonosov Moscow State University, Moscow, Russia., Kirpichnikov MP; Department of Bioengineering, Institute of Bioorganic Chemistry (RAS), Moscow, Russia.; Faculty of Biology, Lomonosov Moscow State University, Moscow, Russia., Trushina DB; Department of X-Ray and Synchrotron Research, A.V. Shubnikov Institute of Crystallography of Federal Scientific Research Centre 'Crystallography and Photonics' of Russian Academy of Sciences, Moscow, Russia., Gasparian ME; Department of Bioengineering, Institute of Bioorganic Chemistry (RAS), Moscow, Russia.
المصدر: Frontiers in cell and developmental biology [Front Cell Dev Biol] 2021 Sep 30; Vol. 9, pp. 733688. Date of Electronic Publication: 2021 Sep 30 (Print Publication: 2021).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Frontiers Media S.A Country of Publication: Switzerland NLM ID: 101630250 Publication Model: eCollection Cited Medium: Print ISSN: 2296-634X (Print) Linking ISSN: 2296634X NLM ISO Abbreviation: Front Cell Dev Biol Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Lausanne : Frontiers Media S.A., [2013]-
مستخلص: Tumor necrosis factor-associated ligand inducing apoptosis (TRAIL) induces apoptosis through the death receptors (DRs) 4 and 5 expressed on the cell surface. Upon ligand stimulation, death receptors are rapidly internalized through clathrin-dependent and -independent mechanisms. However, there have been conflicting data on the role of death receptor endocytosis in apoptotic TRAIL signaling and possible cell type-specific differences in TRAIL signaling have been proposed. Here we have compared the kinetics of TRAIL-mediated internalization and subsequent recycling of DR4 and DR5 in resistant (HT-29 and A549) and sensitive (HCT116 and Jurkat) tumor cell lines of various origin. TRAIL stimulated the internalization of both receptors in a concentration-dependent manner with similar kinetics in sensitive and resistant cell lines without affecting the steady-state expression of DR4 and DR5 in cell lysates. Using the receptor-selective TRAIL variant DR5-B, we have shown that DR5 is internalized independently of DR4 receptor. After internalization and elimination of TRAIL from culture medium, the receptors slowly return to the plasma membrane. Within 4 h in resistant or 6 h in sensitive cells, the surface expression of receptors was completely restored. Recovery of receptors occurred both from newly synthesized molecules or from trans-Golgi network, as cycloheximide and brefeldin A inhibited this process. These agents also suppressed the expression of cell surface receptors in a time- and concentration-dependent manner, indicating that DRs undergo constitutive endocytosis. Inhibition of receptor endocytosis by sucrose led to sensitization of resistant cells to TRAIL and to an increase in its cytotoxic activity against sensitive cells. Our results confirm the universal nature of TRAIL-induced death receptor endocytosis, thus cell sensitivity to TRAIL can be associated with post-endocytic events.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2021 Artykov, Yagolovich, Dolgikh, Kirpichnikov, Trushina and Gasparian.)
التعليقات: Erratum in: Front Cell Dev Biol. 2022 Feb 14;9:820069. (PMID: 35237612)
References: Cancers (Basel). 2019 Jul 07;11(7):. (PMID: 31284696)
Cold Spring Harb Perspect Biol. 2013 Dec 01;5(12):a016949. (PMID: 24296170)
Nat Rev Mol Cell Biol. 2009 Sep;10(9):597-608. (PMID: 19696797)
Cell Death Differ. 2003 Jan;10(1):66-75. (PMID: 12655296)
Results Probl Cell Differ. 2009;49:63-85. (PMID: 19132322)
Elife. 2020 Jan 06;9:. (PMID: 31904339)
Cancer Lett. 2003 May 8;194(1):107-17. (PMID: 12706864)
Lung Cancer. 2009 Jul;65(1):98-104. (PMID: 19081160)
Mol Cancer Res. 2008 Dec;6(12):1861-71. (PMID: 19074831)
Proc Natl Acad Sci U S A. 2017 Jan 17;114(3):504-509. (PMID: 28049841)
J Immunol. 2000 Apr 15;164(8):3961-70. (PMID: 10754286)
Gastroenterology. 2014 Jan;146(1):278-90. (PMID: 24120475)
Cytokine Growth Factor Rev. 2016 Dec;32:63-73. (PMID: 27461871)
Cell Death Dis. 2014 Aug 28;5:e1390. (PMID: 25165876)
Front Cell Dev Biol. 2020 May 19;8:318. (PMID: 32509779)
J Biol Chem. 2013 Mar 1;288(9):6617-28. (PMID: 23300075)
Biochim Biophys Acta Mol Cell Res. 2018 Mar;1865(3):522-531. (PMID: 29278689)
Cell Signal. 2010 Mar;22(3):553-63. (PMID: 19932172)
Cancers (Basel). 2019 Mar 30;11(4):. (PMID: 30935038)
Mol Cancer Ther. 2020 May;19(5):1123-1133. (PMID: 32156787)
Biochemistry (Mosc). 2019 Jun;84(6):627-636. (PMID: 31238862)
Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10283-10288. (PMID: 16801533)
Int J Mol Sci. 2018 Mar 02;19(3):. (PMID: 29498673)
Mol Cell Proteomics. 2012 Mar;11(3):M111.013730. (PMID: 22213832)
Cell Death Dis. 2020 Sep 11;11(9):744. (PMID: 32917855)
J Cell Biol. 1993 Apr;121(1):61-72. (PMID: 8458873)
Cancers (Basel). 2019 Aug 14;11(8):. (PMID: 31416165)
Mol Cell Biol. 2006 Oct;26(19):7046-55. (PMID: 16980609)
J Biol Chem. 2011 Dec 16;286(50):43383-93. (PMID: 22020938)
Oncotarget. 2012 Aug;3(8):833-42. (PMID: 22909995)
J Cell Biol. 2017 Sep 4;216(9):2623-2632. (PMID: 28674108)
PLoS One. 2015 Dec 03;10(12):e0144015. (PMID: 26633016)
Trends Cell Biol. 2006 Dec;16(12):607-9. (PMID: 17064900)
Br J Pharmacol. 2013 Aug;169(8):1723-44. (PMID: 23638798)
Cell Death Dis. 2017 Oct 5;8(10):e3069. (PMID: 28981087)
J Clin Oncol. 2010 Mar 20;28(9):1527-33. (PMID: 20159815)
Arch Pharm Res. 2019 Jan;42(1):88-100. (PMID: 30632113)
Int J Mol Sci. 2013 Jul 11;14(7):14475-503. (PMID: 23852022)
Cancers (Basel). 2020 Apr 30;12(5):. (PMID: 32365976)
Gastroenterology. 2009 Jun;136(7):2365-2376.e1-7. (PMID: 19272388)
Cell Death Differ. 2012 Mar;19(3):523-33. (PMID: 21941373)
Biochim Biophys Acta. 2015 Oct;1848(10 Pt A):2101-10. (PMID: 26055893)
Cancer Biol Ther. 2009 May;8(10):917-22. (PMID: 19270498)
Biochem Biophys Res Commun. 2009 Jan 2;378(1):21-6. (PMID: 18992712)
Mol Biol Cell. 2004 Nov;15(11):5064-74. (PMID: 15356269)
Oncotarget. 2013 Sep;4(9):1349-64. (PMID: 23988408)
J Biol Chem. 2007 Apr 27;282(17):12831-41. (PMID: 17327223)
Apoptosis. 2009 Jun;14(6):778-87. (PMID: 19412666)
Science. 2014 Jul 4;345(6192):98-101. (PMID: 24994655)
فهرسة مساهمة: Keywords: DR4; DR5; TRAIL; brefeldin A; membrane traffic; receptor endocytosis; receptor recycling
تواريخ الأحداث: Date Created: 20211018 Latest Revision: 20220303
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC8514705
DOI: 10.3389/fcell.2021.733688
PMID: 34660590
قاعدة البيانات: MEDLINE
الوصف
تدمد:2296-634X
DOI:10.3389/fcell.2021.733688