Fig. 6
The correlation of HDAC7 and FGF18 expression in NSCLC. a Kaplan–Meier survival analysis of FGF18 expression in 1925 NSCLC cases from the Kaplan–Meier plotter database. b Western blot analysis of FGF18 expression in tumor (T) and paired adjacent nontumor (N) tissues from 12 NSCLC patients. (c) Representative FGF18 IHC images of NSCLC and adjacent non-tumor tissues. Scale bar, 200 μm and 20 μm (inset), respectively. d The IHC analysis of FGF18 expression in 319 NSCLC patients. e Kaplan–Meier survival analysis of FGF18 expression in 319 NSCLC patients. f Correlation analysis of HDAC7 and FGF18 expression in NSCLC tissues. g The comprehensive Kaplan–Meier survival analysis of HDAC7 and FGF18 in 319 NSCLC patients based on the microarray tissue IHC results. h The schematic of a simplified regulatory network involving USP10 and FGF18 in HDAC7-meditated NSCLC progression. USP10 interacts with and stabilizes HDAC7 through deubiquitination, preventing its proteasomal degradation. Elevated HDAC7 expression facilitates β-catenin redistribution to the nucleus by deacetylating β-catenin and inhibiting its phosphorylation. As a result, the nuclear accumulation of β-catenin binds to TCF/LEF to activate the transcription of FGF18 and thus promotes NSCLC proliferation and metastasis