Abstract
The FGF/FGFR signaling axis deregulation of the fibroblast growth factor receptor
(FGFR) family is closely related to tumorigenesis, tumor progression and drug resistance
to anticancer therapy. And fibroblast growth factor receptor 3 (FGFR3) is one member
of this family. In this study, we aimed to investigate the effect of siRNA-induced
knockdown of FGFR3 on the biological behaviors of intrahepatic cholangiocarcinoma
(ICC). The expression levels of FGFR3 were determined in three intrahepatic cholangiocarcinoma
cell lines RBE, HUCCT1 and HCCC9810 cell lines by Western blot. FGFR3 expression in
RBE cell line was knocked down by siRNA. Our study found that knockdown of FGFR3 inhibited
the migration, invasion and proliferation of ICC cells using Wound healing assay,
Transwell migration and invasion assays and Cell proliferation assay. And significantly
down-regulated the protein expression levels of MMP2, cyclinD1, and N Cadherin, but had no significant effect on MMP9, cyclinD3, vimentin, E-cadherin protein.
In addition, we found that ERK/c-Myc presumably is its signaling pathway by bioinformatics
analysis and Western blot verification. To sum up, knockdown of FGFR3 inhibited the
migration, invasion and proliferation of ICC cells. It demonstrated that FGFR3 probably
becomes a therapeutic target for ICC and increases the proportion of potentially curable
intrahepatic cholangiocarcinoma patients treated with FGFR inhibitors.
Keywords
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Article info
Publication history
Published online: August 20, 2022
Accepted:
July 14,
2022
Received:
March 22,
2022
Identification
Copyright
© 2022 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.