Reoxygenation of hypoxic glioblastoma multiforme cells potentiates the killing effect of an interleukin-13-based cytotoxin.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
Tie Fu LiuWaldemar Debinski

Abstract

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. 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. 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 glio...Continue Reading

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Citations

Apr 12, 2014·Neuro-oncology·Bart ThaciSadhak Sengupta
Jun 27, 2014·Journal of Radiation Research·Nina F Jeppesen Edin
Sep 23, 2020·Biomolecules·Antonella AntignaniDavid J FitzGerald
Nov 6, 2020·Neuro-oncology Advances·Puja SharmaWaldemar Debinski

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