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. 2021 Apr 3;11(12):6006–6018. doi: 10.7150/thno.59841

Figure 6.

Figure 6

AKT inhibition is critical for 3-HAA sensitization of HCC to sorafenib. A. The Akt activator SC79 restored HCC cell growth inhibited by the combination of 3-HAA and sorafenib while the ERK activator BCI partially restored HCC cell growth. Cell viability was examined by the CCK8 method. The final concentration of sorafenib and 3-HAA was 5 μM and 50 μM, respectively. The final concentration of SC79 and BCI was 15 μM and 10 μM, respectively. B. The SC79 recovered tumor growth of SMMC7721 xenografts suppressed by the combination treatment. The tumor volumes are presented as mean ± SD. The dose of 3-HAA and sorafenib was 100 mg/Kg.day and 10 mg/Kg.day, respectively. The dose of SC79 was 40 mg/Kg.day. Five mice were recruited in each group. C. The apoptosis detection in xenografts by TUNEL assay. D. The working model for 3-HAA sensitizing sorafenib-resistant HCC cells. 3-HAA-upregulated PPP1R15A/PPP1α dephosphorylate/inactivates Akt which was compensatorily reactivated in sorafenib-resistant HCC cells, and consequently sensitized HCC cells to sorafenib.