Artigo de Periódico
WNT-5A, but not matrix metalloproteinase 3 or b-catenin protein, expression is related to early stages of lip carcinogenesis
Fecha
2009Registro en:
0904-2512
v. 38, n. 9
Autor
Xavier, Flávia Caló de Aquino
Rodini, Camila Oliveira
Ramalho, Luciana Maria Pedreira
Mantesso, Andrea
Nunes, Fabio Daumas
Xavier, Flávia Caló de Aquino
Rodini, Camila Oliveira
Ramalho, Luciana Maria Pedreira
Mantesso, Andrea
Nunes, Fabio Daumas
Institución
Resumen
Oncogenic Wnt/b-catenin signaling
occurs in numerous types of cancers, but little is known
about the role of the Wnt protein family member, WNT-
5A, in lip carcinogenesis. The aim of this study was to
investigate WNT-5A, b-catenin, and matrix metalloproteinase
(MMP)-3 protein expression in actinic cheilitis
(AC), and lip squamous cell carcinoma (LSCC).
METHODS: Twenty-one cases of AC, and fifty-one cases
of LSCC were analyzed, with normal lip mucosa used as a
control. Qualitative and semi-quantitative analyses of
WNT-5A, b-catenin, and MMP-3 immunostaining pattern
and cellular distribution were performed.
RESULTS: WNT-5A was observed in more than 50% of
the cells, scattered in all layers of AC, in contrast to the
absence of immunostaining in normal lip mucosa. AC
presented a higher level of WNT-5A expression than
LSCC (P = 0.0289, Fisher test), while MMP-3 immunoexpression
was statistically more significant in LSCC
than in AC (P = 0.0285, Fisher test). Immunolabeling of
b-catenin protein was differentially distributed between
samples; the majority of AC cases (61.90%) demonstrated
a membranous-cytoplasmic pattern, while a considerable
number of LSCC cases (29.41%) revealed a cytoplasmic
pattern, instead of the usual membranous pattern.
CONCLUSIONS: The present results suggest that
WNT-5A may be an important marker during initial
events of AC malignant transformation, in which noncanonical
and canonical Wnt/b-catenin signaling pathways
could be involved. Additionally, WNT-5A might recruit
other events in LSCC, such as MMP-3 protein synthesis,
as its presence is increased in established malignant
processes without b-catenin dependency.