Death receptor pathways mediate targeted and non-targeted effects of ionizing radiations in breast cancer cells.

Carcinogenesis
Audrey LuceJérôme Lebeau

Abstract

Delayed cell death by mitotic catastrophe is a frequent mode of solid tumor cell death after gamma-irradiation, a widely used treatment of cancer. Whereas the mechanisms that underlie the early gamma-irradiation-induced cell death are well documented, those that drive the delayed cell death are largely unknown. Here we show that the Fas, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and tumor necrosis factor (TNF)-alpha death receptor pathways mediate the delayed cell death observed after gamma-irradiation of breast cancer cells. Early after irradiation, we observe the increased expression of Fas, TRAIL-R and TNF-R that first sensitizes cells to apoptosis. Later, the increased expression of FasL, TRAIL and TNF-alpha permit the apoptosis engagement linked to mitotic catastrophe. Treatments with TNF-alpha, TRAIL or anti-Fas antibody, early after radiation exposure, induce apoptosis, whereas the neutralization of the three death receptors pathways impairs the delayed cell death. We also show for the first time that irradiated breast cancer cells excrete soluble forms of the three ligands that can induce the death of sensitive bystander cells. Overall, these results define the molecular basis of the delayed cell d...Continue Reading

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Citations

Apr 28, 2010·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Caryne Margotto BertolloAlfredo Miranda Goes
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Methods Mentioned

BETA
PCR
electrophoresis
ELISA
PCRs
enzyme-linked immunosorbent assay
X-ray

Software Mentioned

GENORM
Modfit
Sequence Detection System

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