The atypical pattern of cell death in B16F10 melanoma cells treated with TNP-470
(2006) In Cellular & Molecular Biology Letters 11(3). p.384-395- Abstract
- TNP-470 is an acknowledged anti-angiogenic factor, and was studied clinically as an anti-cancer drug. We previously reported on an additional property of this molecule: the intracellular generation of reactive oxygen species in B16F10 melanoma cells. We showed that a massive generation of ROS occurred in the first few hours after treatment with TNP-470 and that this event was critical to subsequent cell death. In this study, we analyzed the process of cell death and noticed an atypical pattern of death markers. Some of these, such as DNA fragmentation or condensation of chromatin, were characteristic for programmed cell death, while others (the lack of phosphatidylserine flip-flop but permeability to propidium iodide, the maintenance of... (More)
- TNP-470 is an acknowledged anti-angiogenic factor, and was studied clinically as an anti-cancer drug. We previously reported on an additional property of this molecule: the intracellular generation of reactive oxygen species in B16F10 melanoma cells. We showed that a massive generation of ROS occurred in the first few hours after treatment with TNP-470 and that this event was critical to subsequent cell death. In this study, we analyzed the process of cell death and noticed an atypical pattern of death markers. Some of these, such as DNA fragmentation or condensation of chromatin, were characteristic for programmed cell death, while others (the lack of phosphatidylserine flip-flop but permeability to propidium iodide, the maintenance of adhesion to the substratum, no change in mitochondrial transmembrane potential, no effect of the panspecific caspase inhibitor) rather suggested a necrotic outcome. We concluded that TNP-470 induced at least some pathways of programmed cell death. However, increasing damage to critical cell functions appears to cause a rapid switch into the necrotic mode. Our data is similar to that in other reports describing the action of ROS-generating agents. We hypothesize that this rapid programmed cell death/necrosis switch is a common scenario following free radical stress. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1135390
- author
- Okroj, Marcin LU ; Stawikowska, Dorota ; Slominska, Ewa M ; Mysliwski, Andrzej and Bigda, Jacek
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Reactive oxygen species, Angiogenesis, Melanoma, Apoptosis
- in
- Cellular & Molecular Biology Letters
- volume
- 11
- issue
- 3
- pages
- 384 - 395
- publisher
- Versita
- external identifiers
-
- pmid:16874459
- scopus:33749345718
- ISSN
- 1689-1392
- DOI
- 10.2478/s11658-006-0032-4
- language
- English
- LU publication?
- no
- id
- e9e2ce62-b2e5-4b0d-9bb3-061b9e881414 (old id 1135390)
- date added to LUP
- 2016-04-01 15:45:07
- date last changed
- 2022-01-28 06:54:52
@article{e9e2ce62-b2e5-4b0d-9bb3-061b9e881414,
abstract = {{TNP-470 is an acknowledged anti-angiogenic factor, and was studied clinically as an anti-cancer drug. We previously reported on an additional property of this molecule: the intracellular generation of reactive oxygen species in B16F10 melanoma cells. We showed that a massive generation of ROS occurred in the first few hours after treatment with TNP-470 and that this event was critical to subsequent cell death. In this study, we analyzed the process of cell death and noticed an atypical pattern of death markers. Some of these, such as DNA fragmentation or condensation of chromatin, were characteristic for programmed cell death, while others (the lack of phosphatidylserine flip-flop but permeability to propidium iodide, the maintenance of adhesion to the substratum, no change in mitochondrial transmembrane potential, no effect of the panspecific caspase inhibitor) rather suggested a necrotic outcome. We concluded that TNP-470 induced at least some pathways of programmed cell death. However, increasing damage to critical cell functions appears to cause a rapid switch into the necrotic mode. Our data is similar to that in other reports describing the action of ROS-generating agents. We hypothesize that this rapid programmed cell death/necrosis switch is a common scenario following free radical stress.}},
author = {{Okroj, Marcin and Stawikowska, Dorota and Slominska, Ewa M and Mysliwski, Andrzej and Bigda, Jacek}},
issn = {{1689-1392}},
keywords = {{Reactive oxygen species; Angiogenesis; Melanoma; Apoptosis}},
language = {{eng}},
number = {{3}},
pages = {{384--395}},
publisher = {{Versita}},
series = {{Cellular & Molecular Biology Letters}},
title = {{The atypical pattern of cell death in B16F10 melanoma cells treated with TNP-470}},
url = {{http://dx.doi.org/10.2478/s11658-006-0032-4}},
doi = {{10.2478/s11658-006-0032-4}},
volume = {{11}},
year = {{2006}},
}