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. 2023 Jan 16;24(2):1776. doi: 10.3390/ijms24021776

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© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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A mechanistic scheme depicting the effects of FGFR3 gene silencing on RAS/mitogen-activated protein kinase (MAPK) signaling and renal pelvis tumorigenesis. Upon stimulation by fibroblast growth factor (FGF), the intracellular tyrosine kinase domain of FGF receptor 3 (FGFR3) may deliver the mitogenic signal through RAS/MAPK cascade and downstream mediator activation, including extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). Hence, FGFR3 overexpression and activation may enhance expression of epithelial–mesenchymal transition (EMT) transcription factors and mediators, which eventually contribute to tumor progression. Our findings suggest that FGFR3 siRNA delivery is a useful strategy for alleviating the RAS/MAPK signaling axis and EMT marker expression in renal pelvis urothelial cells, thereby suppressing their metastatic activity and tumor progression.