دورية أكاديمية
Reoxygenation of hypoxic glioblastoma multiforme cells potentiates the killing effect of an interleukin-13-based cytotoxin.
| العنوان: | Reoxygenation of hypoxic glioblastoma multiforme cells potentiates the killing effect of an interleukin-13-based cytotoxin. |
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| المؤلفون: | Liu TF; Brain Tumor Center of Excellence, Department of Neurosurgery Radiation Oncology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA., Cai J, Gibo DM, Debinski W |
| المصدر: | Clinical cancer research : an official journal of the American Association for Cancer Research [Clin Cancer Res] 2009 Jan 01; Vol. 15 (1), pp. 160-8. |
| نوع المنشور: | Comparative Study; Journal Article; Research Support, N.I.H., Extramural |
| اللغة: | English |
| بيانات الدورية: | Publisher: The Association Country of Publication: United States NLM ID: 9502500 Publication Model: Print Cited Medium: Print ISSN: 1078-0432 (Print) Linking ISSN: 10780432 NLM ISO Abbreviation: Clin Cancer Res Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Denville, NJ : The Association, c1995- |
| مواضيع طبية MeSH: | Cell Hypoxia* , Interleukin-13*, Brain Neoplasms/*metabolism , Cytotoxins/*pharmacology , Diphtheria Toxin/*pharmacology , Glioblastoma/*metabolism , Oxygen/*pharmacology, Brain Neoplasms/therapy ; Cell Line, Tumor ; Furin/analysis ; Glioblastoma/therapy ; Humans ; Immunotoxins/pharmacology ; Interleukin-13 Receptor alpha2 Subunit/metabolism |
| مستخلص: | Purpose: Hypoxia is a cause for resistance to cancer therapies. Molecularly targeted recombinant cytotoxins have shown clinical efficacy in the treatment of patients with primary brain tumors, glioblastoma multiforme, but it is not known whether hypoxia influences their antitumor effect. Experimental Design: We have exposed glioblastoma multiforme cells, such as U-251 MG, U-373 MG, SNB-19, and A-172 MG, to either anoxia or hypoxia and then reoxygenated them while treating with an interleukin (IL)-13-based diphtheria toxin (DT)-containing cytotoxin, DT-IL13QM. We measured the levels of immunoreactive IL-13Ralpha2, a receptor that mediates IL-13-cytotoxin cell killing, and the levels of active form of furin, a protease that activates the bacterial toxin portion in a cytotoxin. Results: We found that anoxia/hypoxia significantly alters the responsiveness of glioblastoma multiforme cells to DT-IL13QM. Interestingly, bringing these cells back to normoxia caused them to become even more susceptible to the cytotoxin than the cells maintained under normoxia. Anoxia/hypoxia caused a highly prominent decrease in the immunoreactive levels of both IL-13R and active forms of furin, and reoxygenation not only restored their levels but also became higher than that in normoxic glioblastoma multiforme cells. Conclusions: Our results show that a recombinant cytotoxin directed against glioblastoma multiforme cells kills these cells much less efficiently under anoxic/hypoxic conditions. The reoxygenation brings unexpected additional benefit of making glioblastoma multiforme cells even more responsive to the killing effect of a cytotoxin. |
| References: | J Biol Chem. 2002 Nov 8;277(45):43194-205. (PMID: 12189139) Proc Natl Acad Sci U S A. 1975 Jun;72(6):2284-8. (PMID: 166383) J Biol Chem. 1990 Nov 25;265(33):20678-85. (PMID: 2122978) Brain Tumor Pathol. 2004;21(1):1-6. (PMID: 15696961) J Biol Chem. 1997 Dec 12;272(50):31707-11. (PMID: 9395513) Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10326-31. (PMID: 11517338) Cancer Res. 2003 Apr 15;63(8):1834-7. (PMID: 12702570) J Neurooncol. 2003 Oct;65(1):3-13. (PMID: 14649881) Protein Eng. 1998 Sep;11(9):811-7. (PMID: 9796831) J Biol Chem. 1996 Dec 13;271(50):32253-9. (PMID: 8943284) Cancer Cell. 2004 Dec;6(6):553-63. (PMID: 15607960) Cancer Invest. 2002;20(5-6):801-9. (PMID: 12197239) Br J Cancer. 2006 Oct 9;95(7):862-8. (PMID: 16953239) Cancer Cell. 2007 Jan;11(1):83-95. (PMID: 17222792) J Biol Chem. 1999 Oct 15;274(42):29944-50. (PMID: 10514477) Clin Cancer Res. 2002 Jun;8(6):1740-6. (PMID: 12060611) Radiother Oncol. 1997 Aug;44(2):171-6. (PMID: 9288846) J Appl Physiol (1985). 2000 Apr;88(4):1474-80. (PMID: 10749844) J Neurooncol. 2007 May;82(3):297-303. (PMID: 17120158) Mol Cell Biol. 2007 Apr;27(8):2997-3007. (PMID: 17283058) Mol Med. 2000 May;6(5):440-9. (PMID: 10952023) Lab Invest. 2006 Dec;86(12):1221-32. (PMID: 17075581) Cancer Res. 1999 Dec 1;59(23):5863-70. (PMID: 10606224) J Biol Chem. 1995 Jul 14;270(28):16775-80. (PMID: 7622490) J Biol Chem. 1993 Feb 5;268(4):2590-4. (PMID: 8381410) J Biol Chem. 1992 Jul 15;267(20):14304-8. (PMID: 1629222) J Neurooncol. 2003 Oct;65(1):15-25. (PMID: 14649882) J Clin Oncol. 2007 Mar 1;25(7):837-44. (PMID: 17327604) J Neurooncol. 2003 Oct;65(1):27-35. (PMID: 14649883) J Biol Chem. 1996 Sep 13;271(37):22428-33. (PMID: 8798406) J Biol Chem. 1994 Dec 16;269(50):31831-5. (PMID: 7989356) J Clin Oncol. 2008 Jan 10;26(2):271-8. (PMID: 18182667) Clin Adv Hematol Oncol. 2007 Nov;5(11):894-902, 907-15. (PMID: 18185489) J Biol Chem. 1991 Jul 5;266(19):12127-30. (PMID: 1905715) Clin Cancer Res. 2004 Dec 15;10(24):8177-84. (PMID: 15623592) Cancer. 2000 Jun 1;88(11):2606-18. (PMID: 10861440) J Neurooncol. 2007 Nov;85(2):133-48. (PMID: 17874037) Clin Cancer Res. 1995 Nov;1(11):1253-8. (PMID: 9815919) Neoplasia. 2002 Sep-Oct;4(5):388-99. (PMID: 12192597) N Engl J Med. 2005 Mar 10;352(10):987-96. (PMID: 15758009) Proc Natl Acad Sci U S A. 1997 May 27;94(11):5667-72. (PMID: 9159130) |
| معلومات مُعتمدة: | R01 CA118261 United States CA NCI NIH HHS |
| المشرفين على المادة: | 0 (Cytotoxins) 0 (Diphtheria Toxin) 0 (Immunotoxins) 0 (Interleukin-13) 0 (Interleukin-13 Receptor alpha2 Subunit) EC 3.4.21.75 (Furin) S88TT14065 (Oxygen) |
| تواريخ الأحداث: | Date Created: 20090102 Date Completed: 20090507 Latest Revision: 20211020 |
| رمز التحديث: | 20240628 |
| مُعرف محوري في PubMed: | PMC3675651 |
| DOI: | 10.1158/1078-0432.CCR-08-2151 |
| PMID: | 19118043 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1078-0432 |
|---|---|
| DOI: | 10.1158/1078-0432.CCR-08-2151 |