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Mice Lacking NCF1 Exhibit Reduced Growth of Implanted Melanoma and Carcinoma Tumors.

Kelkka, Tiina ; Pizzolla, Angela LU ; Laurila, Juha Petteri ; Friman, Tomas ; Gustafsson, Renata LU ; Källberg, Eva LU ; Olsson, Olof ; Leanderson, Tomas LU ; Rubin, Kristofer and Salmi, Marko , et al. (2013) In PLoS ONE 8(12).
Abstract
The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. While the activity of the NOX2 complex is essential for immunity against pathogens and protection against autoimmunity, its role in the development of malignant tumors remains unclear. We compared wild type and Ncf1 (m1J) mutated mice, which lack functional NOX2 complex, in four different tumor models. Ncf1 (m1J) mutated mice developed significantly smaller tumors in two melanoma models in which B16 melanoma cells expressing a hematopoietic growth factor FLT3L or luciferase reporter were used. Ncf1 (m1J) mutated mice developed significantly fewer Lewis Lung Carcinoma (LLC) tumors, but the tumors that did... (More)
The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. While the activity of the NOX2 complex is essential for immunity against pathogens and protection against autoimmunity, its role in the development of malignant tumors remains unclear. We compared wild type and Ncf1 (m1J) mutated mice, which lack functional NOX2 complex, in four different tumor models. Ncf1 (m1J) mutated mice developed significantly smaller tumors in two melanoma models in which B16 melanoma cells expressing a hematopoietic growth factor FLT3L or luciferase reporter were used. Ncf1 (m1J) mutated mice developed significantly fewer Lewis Lung Carcinoma (LLC) tumors, but the tumors that did develop, grew at a pace that was similar to the wild type mice. In the spontaneously arising prostate carcinoma model (TRAMP), tumor growth was not affected. The lack of ROS-mediated protection against tumor growth was associated with increased production of immunity-associated cytokines. A significant increase in Th2 associated cytokines was observed in the LLC model. Our present data show that ROS regulate rejection of the antigenic B16-luc and LLC tumors, whereas the data do not support a role for ROS in growth of intrinsically generated tumors. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
PLoS ONE
volume
8
issue
12
article number
e84148
publisher
Public Library of Science (PLoS)
external identifiers
  • wos:000328735700152
  • pmid:24358335
  • scopus:84892629171
  • pmid:24358335
ISSN
1932-6203
DOI
10.1371/journal.pone.0084148
language
English
LU publication?
yes
id
f19f3c21-5695-4f21-8f9c-548d86feda24 (old id 4223395)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24358335?dopt=Abstract
date added to LUP
2016-04-01 14:16:37
date last changed
2022-01-27 23:45:27
@article{f19f3c21-5695-4f21-8f9c-548d86feda24,
  abstract     = {{The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. While the activity of the NOX2 complex is essential for immunity against pathogens and protection against autoimmunity, its role in the development of malignant tumors remains unclear. We compared wild type and Ncf1 (m1J) mutated mice, which lack functional NOX2 complex, in four different tumor models. Ncf1 (m1J) mutated mice developed significantly smaller tumors in two melanoma models in which B16 melanoma cells expressing a hematopoietic growth factor FLT3L or luciferase reporter were used. Ncf1 (m1J) mutated mice developed significantly fewer Lewis Lung Carcinoma (LLC) tumors, but the tumors that did develop, grew at a pace that was similar to the wild type mice. In the spontaneously arising prostate carcinoma model (TRAMP), tumor growth was not affected. The lack of ROS-mediated protection against tumor growth was associated with increased production of immunity-associated cytokines. A significant increase in Th2 associated cytokines was observed in the LLC model. Our present data show that ROS regulate rejection of the antigenic B16-luc and LLC tumors, whereas the data do not support a role for ROS in growth of intrinsically generated tumors.}},
  author       = {{Kelkka, Tiina and Pizzolla, Angela and Laurila, Juha Petteri and Friman, Tomas and Gustafsson, Renata and Källberg, Eva and Olsson, Olof and Leanderson, Tomas and Rubin, Kristofer and Salmi, Marko and Jalkanen, Sirpa and Holmdahl, Rikard}},
  issn         = {{1932-6203}},
  language     = {{eng}},
  number       = {{12}},
  publisher    = {{Public Library of Science (PLoS)}},
  series       = {{PLoS ONE}},
  title        = {{Mice Lacking NCF1 Exhibit Reduced Growth of Implanted Melanoma and Carcinoma Tumors.}},
  url          = {{https://lup.lub.lu.se/search/files/3886737/4438269}},
  doi          = {{10.1371/journal.pone.0084148}},
  volume       = {{8}},
  year         = {{2013}},
}