Fig 2: Knockdown of CHRF reduces the protein expression level of PI3K/Akt pathway in LAD. Western blotting revealed that knockdown of CHRF decreased the protein expression levels of p-PI3K and p-Akt in (A) SPCA-1 and (B) NCI-H441 cells. Error bars represented the mean ± standard deviation of ≥3 independent experiments. **P<0.01 vs. control group. CHRF, cardiac hypertrophy-related factor; PI3K, posphoinositide-3-kinase; LAD, lung adenocarcinoma; p-, phosphorylated; T-total; si, small interfering RNA; NC, negative control.

Fig 3: UFM1 suppresses epithelial-to-mesenchymal transition of gastric cancer through inactivating AKT/GSK-3β pathway. a The lysates of stable AGS cells were applied to Phospho-Kinase Antibody Array, and pixel densities of indicated proteins were shown in the right panel. b The lysates of stable AGS cells were applied to western blot to detect the expression levels of P110, P85, p-AKT, AKT, p-GSK3βand GSK3β. c The effect of UFM1 stable expression on AGS and HGC-27 cell migration was rescued by LY294002. d Quantitative results of (c) is show. The data are presented as the mean ± SD; scale bar, 50 μm (**, P < 0.01; ns, no significance). e Stable AGS cells were treated with DMSO or LY294002. Then cell lysates were applied in western blot analysis

Fig 4: Apoptotic effect of miRNA-21-5p was determined via regulating PI3K/Akt/FOXO1 signaling. PI3K, AKT and p-FOXO1 protein expression levels were measured using western blot analysis. Inhibition of miRNA21-5p suppressed the PI3K/Akt/FOXO1 signaling pathway. Experiments were performed in triplicate. miRNA, microRNA; FOXO1, Forkhead Box O1; p-FOXO1, phosphorylated Forkhead Box O1.

Fig 5: HOTAIR competitively binds to miR‐206, thereby promoting STC2 expression, activating PI3K/AKT signalling pathway