Mechanism of FKBP10 promoting proliferation and migration of gastric cancer cells

Objective To investigate the regulative role of FKBP10 in the progression of gastric cancer and the underlying mechanism. Methods Bioinformatics analysis was applied to detect the expression of FKBP10 in gastric cancer samples and normal samples, as well as analyze its relationship with prognosis. qRT-PCR and Western blotting were employed to measure its expression at mRNA and protein levels in gastric cancer cell lines BGC823, MGC803, SGC7901, MKN45 and AGS and human gastric epithelial cell line GES. Then colony formation and transwell assay were conducted to detect the effect of its down-regulation on the proliferation and migration of the cells. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was used to reveal the FKBP10 involved signaling pathways, which was verified by Western blotting. Results FKBP10 was up-regulated in gastric cancer cell lines than the GES cells. Knockdown of FKBP10 by siRNA restricted the proliferative and migrative abilities of gastric cancer cells. KEGG analysis indicated that FKBP10 may be involved in the process of epithelial-mesenchymal transition (EMT) and TGF-β played important role in the process. Western blotting showed that down-regulation of FKBP10 resulted in increased expression of epithelial related biomarkers while decreased expression of mesenchymal related biomarkers, then the expression of p-SMAD2/3 were reduced simultaneously. Conclusion FKBP10 promotes the proliferation and migration of gastric cancer via regulating EMT and TGF-β/SMAD signaling pathway.