دورية أكاديمية
أعرض في EDS

G3BP1 knockdown sensitizes U87 glioblastoma cell line to Bortezomib by inhibiting stress granules assembly and potentializing apoptosis.

التفاصيل البيبلوغرافية
العنوان: G3BP1 knockdown sensitizes U87 glioblastoma cell line to Bortezomib by inhibiting stress granules assembly and potentializing apoptosis.
المؤلفون: Bittencourt LFF; Departamento de Fisiologia E Biofísica, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Av. Antônio Carlos, 6627 - Pampulha, Belo Horizonte, MG, 31270-901, Brazil., Negreiros-Lima GL; Faculdade de Farmácia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Grais, Brazil., Sousa LP; Faculdade de Farmácia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Grais, Brazil., Silva AG; Laboratório de Patologia Experimental, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, Minas Gerais, Brazil., Souza IBS; Laboratório de Patologia Experimental, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, Minas Gerais, Brazil., Ribeiro RIMA; Laboratório de Patologia Experimental, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, Minas Gerais, Brazil., Dutra MF; Departamento de Fisiologia E Biofísica, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Av. Antônio Carlos, 6627 - Pampulha, Belo Horizonte, MG, 31270-901, Brazil., Silva RF; Departamento de Fisiologia E Biofísica, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Av. Antônio Carlos, 6627 - Pampulha, Belo Horizonte, MG, 31270-901, Brazil., Dias ACF; Departamento de Fisiologia E Biofísica, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Av. Antônio Carlos, 6627 - Pampulha, Belo Horizonte, MG, 31270-901, Brazil., Soriani FM; Departamento de Biologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais (UFMG), Minas Gerais, Brazil., Martins WK; Universidade Anhanguera de São Paulo, Pós-graduação Stricto-sensu e Pesquisa, São Paulo, Brazil., Barcelos LS; Departamento de Fisiologia E Biofísica, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Av. Antônio Carlos, 6627 - Pampulha, Belo Horizonte, MG, 31270-901, Brazil. luciolasbarcelos@gmail.com.
المصدر: Journal of neuro-oncology [J Neurooncol] 2019 Sep; Vol. 144 (3), pp. 463-473. Date of Electronic Publication: 2019 Aug 07.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Springer Country of Publication: United States NLM ID: 8309335 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1573-7373 (Electronic) Linking ISSN: 0167594X NLM ISO Abbreviation: J Neurooncol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2005- : New York : Springer
Original Publication: Boston : M. Nijhoff, 1983-
مواضيع طبية MeSH: Antineoplastic Agents/*pharmacology , Apoptosis/*drug effects , Bortezomib/*pharmacology , Cytoplasmic Granules/*drug effects , DNA Helicases/*antagonists & inhibitors , Glioblastoma/*drug therapy , Neovascularization, Pathologic/*drug therapy , Poly-ADP-Ribose Binding Proteins/*antagonists & inhibitors , RNA Helicases/*antagonists & inhibitors , RNA Recognition Motif Proteins/*antagonists & inhibitors, Antineoplastic Agents, Alkylating/pharmacology ; Cell Proliferation/drug effects ; Cytoplasmic Granules/pathology ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Temozolomide/pharmacology ; Tumor Cells, Cultured
مستخلص: Introduction: Glioblastoma multiforme (GBM) is the most lethal form of gliomas. New therapies are currently in development to tackle treatment limitations such as chemotherapy resistance. One mechanism of resistance may be the stress granules (SG) assembly, a stress-related cellular response that allows cells to recruit and protect mRNAs during stress. SG are composed of various proteins, being G3BP1 a core element that enucleates and results in SG assembly. Here, we aimed to evaluate the effects of inhibiting the G3PB1 expression in the chemotherapeutical-induced cell death of the U87 glioblastoma cell line.
Materials and Methods: G3BP1 mRNA and protein expression were modulated with short-interference RNA (siRNA). The viability of U87 cells after Bortezomib (BZM), a proteasome inhibitor, and Temozolomide (TMZ), an alkylating agent, was assessed by MTT assay. Apoptosis was evaluated by staining cells with Annexin-V/7-AAD and analyzing by flow cytometry. Caspase-3 activation was evaluated by immunoblotting. The chorioallantoic membrane in vivo assay was used to evaluate angiogenesis.
Results: When G3BP1 was knocked-down, the SG assembly was reduced and the BZM-treated cells, but not TMZ-treated cells, had a significant increase in the apoptotic response. Corroborating this data, we observed increased Caspase-3 activation in the BZM-treated and G3BP1-knocked-down cells when compared to vehicle-treated and scramble-transfected cells. Worth mentioning, the conditioned culture medium of G3BP1-knocked-down BZM-treated cells inhibited angiogenesis when compared to controls.
Conclusion: Our data suggest G3BP1 knockdown diminishes SG formation and stimulates BZM-induced apoptosis of U87 cells in vitro, in addition to inhibiting glioblastoma-induced angiogenesis in vivo.
التعليقات: Erratum in: J Neurooncol. 2019 Sep 2;:. (PMID: 31478154)
References: Oncologist. 1999;4(3):209-24. (PMID: 10394589)
J Cell Biol. 1999 Dec 27;147(7):1431-42. (PMID: 10613902)
Mol Cell. 2000 May;5(5):897-904. (PMID: 10882126)
Drug Discov Today. 2003 Apr 1;8(7):307-15. (PMID: 12654543)
J Biol Chem. 2005 Apr 29;280(17):16925-33. (PMID: 15684421)
BMC Bioinformatics. 2006 Mar 09;7:123. (PMID: 16526949)
J Microsc. 2006 Dec;224(Pt 3):213-32. (PMID: 17210054)
Biochem Biophys Res Commun. 2007 Oct 19;362(2):225-9. (PMID: 17707767)
EMBO J. 2007 Dec 12;26(24):5020-32. (PMID: 18034160)
Nat Cell Biol. 2008 Nov;10(11):1324-32. (PMID: 18836437)
Cancer Sci. 2009 Dec;100(12):2235-41. (PMID: 19737147)
Cancer Cell Int. 2010 Apr 29;10:12. (PMID: 20429927)
Toxicol In Vitro. 1996 Aug;10(4):431-46. (PMID: 20650224)
Brain Tumor Pathol. 2011 Feb;28(1):13-24. (PMID: 21221826)
PLoS One. 2011;6(5):e20254. (PMID: 21637851)
Front Pharmacol. 2011 Aug 25;2:49. (PMID: 21904528)
Cancer Cell. 2011 Sep 13;20(3):384-99. (PMID: 21907928)
Cancer Sci. 2012 Oct;103(10):1848-56. (PMID: 22703643)
Biochem Biophys Res Commun. 2012 Jul 13;423(4):763-9. (PMID: 22705549)
Leuk Lymphoma. 2013 May;54(5):1061-8. (PMID: 23025401)
PLoS Genet. 2013;9(1):e1003169. (PMID: 23341773)
Cell Death Dis. 2013 Jul 11;4:e725. (PMID: 23846227)
J Neurosurg. 2013 Dec;119(6):1415-23. (PMID: 24093630)
Nat Rev Drug Discov. 2013 Dec;12(12):931-47. (PMID: 24287781)
Adv Healthc Mater. 2014 Aug;3(8):1182-93. (PMID: 24577795)
Neuro Oncol. 2014 Jul;16(7):896-913. (PMID: 24842956)
Methods Mol Biol. 2015;1219:1-9. (PMID: 25308257)
Pharmacogenet Genomics. 2014 Dec;24(12):582-7. (PMID: 25322287)
Lab Chip. 2015 Jan 7;15(1):301-10. (PMID: 25370780)
RNA Biol. 2014;11(8):1019-30. (PMID: 25531407)
Oncol Rep. 2015 May;33(5):2277-84. (PMID: 25812695)
Oncotarget. 2015 Jul 10;6(19):17039-53. (PMID: 25962958)
Nat Rev Genet. 2015 Sep;16(9):543-52. (PMID: 26281785)
Exp Ther Med. 2015 Sep;10(3):1219-1223. (PMID: 26622468)
J Neurooncol. 2016 Apr;127(2):253-60. (PMID: 26732083)
Nat Commun. 2016 Jan 07;7:10252. (PMID: 26738979)
Oncotarget. 2016 May 24;7(21):30307-22. (PMID: 27083003)
J Cell Biol. 2016 Nov 7;215(3):313-323. (PMID: 27821493)
Int J Oncol. 2017 Feb;50(2):477-486. (PMID: 28000897)
J Neuropathol Exp Neurol. 2017 Dec 1;76(12):1000-1007. (PMID: 29136455)
Biomed Pharmacother. 2018 Jul;103:482-489. (PMID: 29677533)
Oncol Rep. 2018 Jun;39(6):2873-2880. (PMID: 29693175)
Int J Radiat Oncol Biol Phys. 2018 Apr 1;100(5):1195-1203. (PMID: 29722661)
Genes Dis. 2016 May 11;3(3):198-210. (PMID: 30258889)
Cell Physiol Biochem. 2018;51(6):2536-2546. (PMID: 30562758)
Blood Adv. 2019 Jan 8;3(1):51-62. (PMID: 30617217)
معلومات مُعتمدة: 2013/07937-8 FAPESP (Fundação de Amparo à Pesquisa do Estado de São Paulo); 2013/07937-8 FAPESP (Fundação de Amparo à Pesquisa do Estado de São Paulo); 304394/2018-1 CNPq (Conselho Nacional de Pesquisa); ADRC12/2011 PRPq/UFMG (Pró-Reitoria de Pesquisa da UFMG)
فهرسة مساهمة: Keywords: Angiogenesis; Apoptosis; Bortezomib; G3BP1; Glioblastoma multiforme; Stress granules
المشرفين على المادة: 0 (Antineoplastic Agents)
0 (Antineoplastic Agents, Alkylating)
0 (Poly-ADP-Ribose Binding Proteins)
0 (RNA Recognition Motif Proteins)
69G8BD63PP (Bortezomib)
EC 3.6.4.- (DNA Helicases)
EC 3.6.4.12 (G3BP1 protein, human)
EC 3.6.4.13 (RNA Helicases)
YF1K15M17Y (Temozolomide)
تواريخ الأحداث: Date Created: 20190809 Date Completed: 20200214 Latest Revision: 20200225
رمز التحديث: 20231215
DOI: 10.1007/s11060-019-03252-6
PMID: 31392596
قاعدة البيانات: MEDLINE
الوصف
تدمد:1573-7373
DOI:10.1007/s11060-019-03252-6