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. 2021 Sep 23;46(5):240. doi: 10.3892/or.2021.8191

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Copyright: © Wang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 7. — Overexpression of CHAC1 sensitizes PLC cells to DHA. Si*CHAC1 exclusively targeting the 3′ untranslated region was used to knockdown endogenous CHAC1 expression. (A and D) Knockdown of CHAC1 was assessed using western blotting. (B and E) Cell viability and (C and F) MDA levels were determined. Data are presented as the mean ± standard deviation of four repeats. *P<0.05, **P<0.01, ***P<0.001 vs. control. DHA, dihydroartemisinin; siRNA, small interfering RNA; NC, negative control; CHAC1, ChaC glutathione specific γ-glutamylcyclotransferase 1; PLC, primary liver cancer; MDA, malondialdehyde.