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. 2023 Nov 16;9:416. doi: 10.1038/s41420-023-01664-y

Fig. 4. The antitumor efficacy of aspirin plus lenvatinib depends on its regulation of multiple oncogenes and tumor suppressors.

Fig. 4

a–c HepG2 and Hepa1-6 Cells were separately treated with control solution, 4 mM aspirin, 10 μM lenvatinib, or aspirin (4 mM) plus lenvatinib (10 μM) for 48 h. Western Blotting assays were used to detect the effects of different drugs on a the phosphorylation of AKT, MEK, and ERK, which regulated the activities of Ras/Raf/MAPK and PI3K/AKT pathways; b the expression of proteins associated with the cell cycle (P21, P27 and the phosphorylation of Rb and CDK2); c the expression of proteins related to cell metabolism (c-Myc, LDHA), the activity of AMPK/mTOR pathway (the phosphorylation of AMPK, 4EBP1) and immunoregulation (COX2). d CCK8 assays reveal the effect of AKT activation on cell viability of HCC cells mediated by the drug combination. e Representative micrographs for the EdU assays show the effect of AKT activation on cell proliferation of HCC cells mediated by the drug combination. f Cell cycle detection assays display the effect of AKT activation on the growth inhibition of drug combination on HepG2 and Hepa1-6 cells. g–i CCK8 assays (g), EdU assays (h), and cell cycle detection assays (i) show the effect of c-Myc overexpression on the decrease in cell viability, growth inhibition and cell cycle arrest induced by aspirin plus lenvatinib. j–l CCK8 assays (j), EdU assays (k), and cell cycle detection assays (l) reveal the effect of p21 silencing on the antitumor efficacy mediated by aspirin plus lenvatinib. Error bars represent the means of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001.