Fig. 7

MIR194-2HG inhibited GC progression via the miR-194/miR-192-BTF3L4 axis. (A) BTF3L4 expression was significantly upregulated in GC according to the RNA-seq data in the TCGA_STAD cohort. (B) BTF3L4 expression was significantly upregulated in GC according to the RNA-seq data in the GSE122401 cohort. (C, D) BTF3L4 expression was positively correlated with poor differentiation (G-stages) and malignant progression (T-stages) of GC. (E) BTF3L4 overexpression predicted a poor relapse-free survival in the TCGA_STAD cohort. (F) BTF3L4 overexpression predicted poor prognosis in GSE62254 cohort. (G, H) Knockdown of MIR194-2HG significantly upregulated mRNA and protein levels of BTF3L4 in GC cell lines. (I, J) Knockdown of BTF3L4 restored the promoting effect of MIR194-2HG depletion on the proliferation of GC cell lines. (K, L) Knockdown of BTF3L4 partially restored the promoting effect of MIR194-2HG depletion on the invasion of GC cell lines