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00925njm 22002777a 4500 dc Quintanal-Villalonga, Alvaro author Ojeda-Marquez, Laura author Marrugal, Ángela author Yagüe, Patricia author Ponce-Aix, Santiago author Salinas, Ana author Carnero, Amancio author Ferrer, Irene author Molina-Pinelo, Sonia author Paz Ares , Luis Gonzaga author 2018 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. Sci Rep. 2018; 8(1):2394. 10.1038/s41598-018-20570-3 2045-2322 2045-2322 Scientific reports 29402970 http://hdl.handle.net/20.500.12105/6621 FACTOR RECEPTOR 4 EPITHELIAL-MESENCHYMAL TRANSITION; FGFR4 GLY388ARG POLYMORPHISM EXTRAHEPATIC CHOLANGIOCARCINOMA; HEPATOCELLULAR-CARCINOMA; PROGNOSTIC-SIGNIFICANCE ARG(388) ALLELE SURVIVAL CELLS STAT3 The FGFR4-388arg Variant Promotes Lung Cancer Progression by N-Cadherin Induction