| dc.description.abstract | Oral carcinogenesis is a complex and multifactorial process that involves cumulative
genetic and molecular alterations, leading to uncontrolled cell proliferation, impaired DNA repair
and defective cell death. At the early stages, the onset of potentially malignant lesions in the
oral mucosa, or oral dysplasia, is associated with higher rates of malignant progression towards
carcinoma in situ and invasive carcinoma. E orts have been made to get insights about signaling
pathways that are deregulated in oral dysplasia, as these could be translated into novel markers
and might represent promising therapeutic targets. In this context, recent evidence underscored the
relevance of the Wnt/ -catenin signaling pathway in oral dysplasia, as this pathway is progressively
“switched on” through the di erent grades of dysplasia (mild, moderate and severe dysplasia),
with the consequent nuclear translocation of -catenin and expression of target genes associated
with the maintenance of representative traits of oral dysplasia, namely cell proliferation and
viability. Intriguingly, recent studies provide an unanticipated connection between active -catenin
signaling and deregulated endosome tra cking in oral dysplasia, highlighting the relevance of
endocytic components in oral carcinogenesis. This review summarizes evidence about the role of
the Wnt/ -catenin signaling pathway and the underlying mechanisms that account for its aberrant
activation in oral carcinogenesis. | |
