Figure 5.
CES2 represses the PI3K/AKT/MYC signaling pathway and induces apoptotic signaling in OSCC. (A, B) A volcano plot (A) and GSEA (B) showing the transcriptome differences between patients with CES2high (n = 110) and CES2low (n = 239) in the TCGA cohort. (C–E) RNA-seq profiling was performed with stably empty vector- and CES2-overexpressing cells. The volcano plot (C), GSEA (D) and GO analysis (E) showing the transcriptome differences between stably empty vector- and CES2-overexpressing cells. (F) Pathways of the differentially expressed genes and/or lipids between CES2- and empty vector-overexpressing cells as identified by MetaboAnalyst 5.0 based on lipidomic and RNA-seq data. (G) Representative levels of PIs as determined by ELISAs with CAL33 and UM1 cells in which CES2 or the empty vector was overexpressed. (H–J) The protein levels of the PI3K/AKT/MYC signaling pathway, including p-AKT (Thr308 and Ser473), p-mTOR (Ser2448), p-GSK3β (Ser9) and MYC (H); EMT markers, including E-cadherin and Vimentin (I); and endogenous apoptosis markers, including cleaved PARP, cleaved caspase 3 and cytochrome C (J), were measured by western blotting. β-Actin was used as the loading control. The mean ± s.d.; ∗, P < 0.05; Student’s t tests.