RT Journal Article
T1 The FGFR4-388arg Variant Promotes Lung Cancer Progression by N-Cadherin Induction.
A1 Quintanal-Villalonga, Álvaro
A1 Ojeda-Márquez, Laura
A1 Marrugal, Ángela
A1 Yagüe, Patricia
A1 Ponce-Aix, Santiago
A1 Salinas, Ana
A1 Carnero, Amancio
A1 Ferrer, Irene
A1 Molina-Pinelo, Sonia
A1 Paz-Ares, Luis
AB The FGFR4-388Arg variant has been related to poor prognosis in several types of cancer, including lung cancer. The mechanism underlying this association has not been addressed in detail in patients with this pathology. Here, we report that this FGFR4 variant induces MAPK and STAT3 activation and causes pro-oncogenic effects in NSCLC in vitro and in vivo. This variant induces the expression of EMT-related genes, such as N-cadherin, vimentin, Snail1 and Twist1. Indeed, the induction of N-cadherin protein expression by this variant is essential for its pro-tumorigenic role. The presence of the FGFR4-388Arg variant correlates with higher N-cadherin expression levels in clinical NSCLC samples and with poorer outcome in patients with FGFR expression. These results support the prognostic role of this FGFR variant in lung cancer and show that these effects may be mediated by the induction of N-cadherin expression and an EMT phenotype.
YR 2018
FD 2018-02-05
LK http://hdl.handle.net/10668/12085
UL http://hdl.handle.net/10668/12085
LA en
DS RISalud
RD Apr 17, 2025