IGF1/IGF-1R promotes hepatocellular carcinoma progression by activating the Akt/GSK-3β pathway
Fig 5
Reversal of IGF-1R’s Effects on HCC by suppressing Akt/GSK-3β (A, B,C).
The protein levels of p-Akt, p-GSK-3β, Snail, E-cadherin, and N-cadherin across experimental groups (*P < 0.05, **P < 0.01, ***P < 0.001). (D, E) Differences in the proliferation capacity of each group via the EdU assay (**P < 0.01, ***P < 0.001). (F, G) Cell proliferation ability of each cell group in the clone formation assay (*P < 0.05, **P < 0.01). (H, I) Transwell assay to determine the cell migration ability of each group (*P < 0.05, **P < 0.01). (J, K) Cell migration ability of each group. (L, M) Apoptotic capacity of each group via the JC-1 assay (*P < 0.05, **P < 0.01). All data are expressed as mean ± standard deviation from at least three independent experiments. Comparisons between two groups were analyzed using a two-tailed Student’s t-test. Comparisons among multiple groups were analyzed via one-way analysis of variance followed by Tukey’s post-hoc test. A P-value of <0.05 was considered statistically significant. Error bars represent SEM, and statistical significance is indicated in the figures.