Publication: The receptor for advanced glycation end products is dispensable in a mouse model of oral and esophageal carcinogenesis
Authors
Mark, Regina ; Lorenzo Bermejo, Justo ; Bierhaus, Angelika ; Plinker, Peter K ; Angel, Peter ; Hess, Jochen
item.page.secondaryauthor
item.page.director
Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Aberrant expression of the receptor for
advanced glycation end products (RAGE) and its
ligands, such as S100/Calgranulins, has been
demonstrated in squamous cell carcinomas of the upper
aerodigestive tract. However, the question whether
RAGE signaling is causally linked with neoplastic
transformation of keratinocytes in mucosal epithelia has
not been addressed so far. We used the well-established
mouse model of 4-nitroquinoline-1-oxide (4-NQO)
induced tumorigenesis to investigate tumor development
in control and RAGE-deficient (Rage-/-
) animals.
Although 4-NQO induced lesions of the tongue and the
esophagus showed strong induction of the RAGE
ligands S100a8 and S100a9, we did not observe any
significant difference in tumor incidence or multiplicity
between control and Rage-/- mice. Furthermore, detailed
analysis of tumor sections by histological and
immunohistochemical staining revealed no difference in
either the size or histological architecture of dysplastic
lesions, tumor cell proliferation, or the number of
inflammatory immune cells in the tumor microenvironment.
Finally, we detected induced transcript and
protein levels of the Toll-like receptor 4 (Tlr4) in 4-NQO
induced lesions, suggesting that signaling via the S100-
Tlr4 axis may compensate for the lack of RAGE in early
stages of tumor development.
publication.page.subject
Citation
Histology and Histopathology, vol. 28, nº 12 (2013)
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.