دورية أكاديمية

The Interleukin-11/IL-11 Receptor Promotes Glioblastoma Survival and Invasion under Glucose-Starved Conditions through Enhanced Glutaminolysis.

التفاصيل البيبلوغرافية
العنوان: The Interleukin-11/IL-11 Receptor Promotes Glioblastoma Survival and Invasion under Glucose-Starved Conditions through Enhanced Glutaminolysis.
المؤلفون: Stuart SF; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia.; Fiona Elsey Cancer Research Institute, Ballarat, VIC 3350, Australia., Bezawork-Geleta A; Department of Physiology, The University of Melbourne, Melbourne, VIC 3010, Australia., Areeb Z; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia., Gomez J; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia., Tsui V; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia., Zulkifli A; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia., Paradiso L; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia., Jones J; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia.; Department of Neurosurgery, The Royal Melbourne Hospital, Parkville, VIC 3050, Australia., Nguyen HPT; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia., Putoczki TL; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia.; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3050, Australia.; Department of Medical Biology, The University of Melbourne, Parkville, VIC 3050, Australia., Licciardi PV; Murdoch Children's Research Institute, Melbourne, VIC 3052, Australia.; Department of Paediatrics, The University of Melbourne, Melbourne, VIC 3052, Australia., Kannourakis G; Fiona Elsey Cancer Research Institute, Ballarat, VIC 3350, Australia.; Health, Innovation and Transformation Centre, Federation University, Ballarat, VIC 3350, Australia., Morokoff AP; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia.; Department of Neurosurgery, The Royal Melbourne Hospital, Parkville, VIC 3050, Australia., Achuthan AA; Department of Medicine, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia., Luwor RB; Department of Surgery, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia.; Fiona Elsey Cancer Research Institute, Ballarat, VIC 3350, Australia.; Health, Innovation and Transformation Centre, Federation University, Ballarat, VIC 3350, Australia.
المصدر: International journal of molecular sciences [Int J Mol Sci] 2023 Feb 08; Vol. 24 (4). Date of Electronic Publication: 2023 Feb 08.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI, [2000-
مواضيع طبية MeSH: Glioblastoma*/metabolism, Humans ; Cell Line ; Cell Line, Tumor ; Glucose/metabolism ; Interleukin-11/metabolism ; Receptors, Interleukin-11
مستخلص: Glioblastoma cells adapt to changes in glucose availability through metabolic plasticity allowing for cell survival and continued progression in low-glucose concentrations. However, the regulatory cytokine networks that govern the ability to survive in glucose-starved conditions are not fully defined. In the present study, we define a critical role for the IL-11/IL-11Rα signalling axis in glioblastoma survival, proliferation and invasion when cells are starved of glucose. We identified enhanced IL-11/IL-11Rα expression correlated with reduced overall survival in glioblastoma patients. Glioblastoma cell lines over-expressing IL-11Rα displayed greater survival, proliferation, migration and invasion in glucose-free conditions compared to their low-IL-11Rα-expressing counterparts, while knockdown of IL-11Rα reversed these pro-tumorigenic characteristics. In addition, these IL-11Rα-over-expressing cells displayed enhanced glutamine oxidation and glutamate production compared to their low-IL-11Rα-expressing counterparts, while knockdown of IL-11Rα or the pharmacological inhibition of several members of the glutaminolysis pathway resulted in reduced survival (enhanced apoptosis) and reduced migration and invasion. Furthermore, IL-11Rα expression in glioblastoma patient samples correlated with enhanced gene expression of the glutaminolysis pathway genes GLUD1, GSS and c-Myc. Overall, our study identified that the IL-11/IL-11Rα pathway promotes glioblastoma cell survival and enhances cell migration and invasion in environments of glucose starvation via glutaminolysis.
References: Genes Dev. 2011 May 15;25(10):1041-51. (PMID: 21576264)
Cytokine Growth Factor Rev. 2015 Oct;26(5):489-98. (PMID: 26209885)
Cancer Res. 2009 Oct 15;69(20):7986-93. (PMID: 19826036)
Clin Cancer Res. 2017 Oct 15;23(20):6292-6304. (PMID: 28720668)
J Cell Biochem. 2019 Oct;120(10):16824-16839. (PMID: 31111555)
Cell Metab. 2012 Jan 4;15(1):110-21. (PMID: 22225880)
Oncogene. 2020 Apr;39(14):2975-2986. (PMID: 32034306)
Nutr Metab (Lond). 2005 Oct 21;2:30. (PMID: 16242042)
Mol Med Rep. 2018 Mar;17(3):3972-3978. (PMID: 29286137)
Methods. 2001 Dec;25(4):402-8. (PMID: 11846609)
PLoS One. 2014 Mar 19;9(3):e92444. (PMID: 24647355)
J Biol Chem. 2020 Jun 12;295(24):8285-8301. (PMID: 32332100)
Cancer Cell. 2010 Sep 14;18(3):207-19. (PMID: 20832749)
Exp Cell Res. 2018 Jul 15;368(2):184-193. (PMID: 29709516)
Oncogene. 2016 Jun 16;35(24):3201-8. (PMID: 26455325)
Biology (Basel). 2017 Feb 08;6(1):. (PMID: 28208702)
Cell Metab. 2012 Jun 6;15(6):827-37. (PMID: 22682223)
Nat Cell Biol. 2015 Dec;17(12):1556-68. (PMID: 26595383)
Oncol Lett. 2018 Oct;16(4):4095-4104. (PMID: 30250528)
Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19345-50. (PMID: 18032601)
J Neurooncol. 2011 Apr;102(2):317-21. (PMID: 20683757)
BMC Cancer. 2021 Jan 20;21(1):83. (PMID: 33472598)
Annu Rev Biomed Eng. 2017 Jun 21;19:163-194. (PMID: 28301735)
Cells. 2020 May 18;9(5):. (PMID: 32443613)
Cells. 2019 Dec 18;9(1):. (PMID: 31861356)
Mol Cell. 2014 Oct 23;56(2):205-218. (PMID: 25242145)
Front Oncol. 2018 Aug 24;8:333. (PMID: 30197878)
Mol Cell. 2014 Nov 6;56(3):414-424. (PMID: 25458842)
Mol Syst Biol. 2014 May 05;10:728. (PMID: 24799285)
Mol Cancer Ther. 2016 Nov;15(11):2609-2619. (PMID: 27535971)
Clin Cancer Res. 2016 Sep 1;22(17):4452-65. (PMID: 27076630)
Biochim Biophys Acta Mol Cell Res. 2017 Nov;1864(11 Pt B):2105-2117. (PMID: 28630024)
Cancers (Basel). 2021 Nov 29;13(23):. (PMID: 34885110)
Genes Dev. 2007 Nov 1;21(21):2683-710. (PMID: 17974913)
Cell Metab. 2019 Aug 6;30(2):274-289.e5. (PMID: 31056285)
Cell Death Dis. 2019 Apr 30;10(5):353. (PMID: 31040267)
J Clin Invest. 2008 May;118(5):1727-38. (PMID: 18431520)
Onco Targets Ther. 2019 Mar 28;12:2397-2408. (PMID: 30992675)
Trends Biochem Sci. 2010 Aug;35(8):427-33. (PMID: 20570523)
Cell Metab. 2011 Dec 7;14(6):724-38. (PMID: 22152301)
Cancers (Basel). 2018 Dec 19;10(12):. (PMID: 30572654)
Cell Metab. 2019 Aug 6;30(2):229-230. (PMID: 31390546)
Clin Cancer Res. 2009 Oct 1;15(19):6002-7. (PMID: 19755387)
Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18782-7. (PMID: 19033189)
EMBO Mol Med. 2019 Apr;11(4):. (PMID: 30885958)
J Clin Invest. 2015 Apr;125(4):1591-602. (PMID: 25798620)
Int J Mol Sci. 2015 Sep 22;16(9):22830-55. (PMID: 26402672)
Curr Mol Med. 2013 May;13(4):514-34. (PMID: 22934847)
J Exp Clin Cancer Res. 2019 Feb 8;38(1):63. (PMID: 30736824)
J Biol Chem. 2008 Jul 25;283(30):20621-7. (PMID: 18364355)
Cold Spring Harb Perspect Med. 2013 Aug 01;3(8):. (PMID: 23906881)
Cancers (Basel). 2019 Oct 24;11(11):. (PMID: 31652923)
Exp Mol Med. 2020 Sep;52(9):1496-1516. (PMID: 32943735)
Cancer Cell. 2013 Aug 12;24(2):257-71. (PMID: 23948300)
BMC Biotechnol. 2012 Mar 21;12:8. (PMID: 22433466)
Nature. 2009 Apr 9;458(7239):762-5. (PMID: 19219026)
Semin Immunol. 2014 Feb;26(1):54-74. (PMID: 24552665)
Nat Neurosci. 2013 Oct;16(10):1373-82. (PMID: 23995067)
Front Immunol. 2014 Feb 19;5:58. (PMID: 24600449)
معلومات مُعتمدة: NA Rebecca L. Cooper Medical Research Foundation; NA International Foundation for Ethical Research
فهرسة مساهمة: Keywords: IL-11; glioblastoma; glutaminolysis; invasion; survival
المشرفين على المادة: IY9XDZ35W2 (Glucose)
0 (Interleukin-11)
0 (Receptors, Interleukin-11)
0 (IL11 protein, human)
تواريخ الأحداث: Date Created: 20230225 Date Completed: 20230301 Latest Revision: 20230301
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC9960532
DOI: 10.3390/ijms24043356
PMID: 36834778
قاعدة البيانات: MEDLINE
الوصف
تدمد:1422-0067
DOI:10.3390/ijms24043356