Fig. 2: PID1 reduced efficacy of chemotherapeutic agents but facilitated Sorafenib-induced apoptosis.
A Seahorse analysis was performed to evaluate the capacity of mitochondria respiration in HepG2 cells with or without PID1 overexpression upon H2O2 (200 μM) treatment for 12 h, basal respiration rate and maximum respiration rate were calculated. B–C Mitochondrial membrane potential in HepG2 cells and Hepa1–6 cells with or without PID1 overexpression upon treatment of three anticancer agents was detected by cytometry analysis and Red/Green ratio was calculated. D–E HepG2 cells and Hepa1–6 cells were treated with Cisplatin (20 μM), Doxorubicin (200 nM) and Gemcitabine (20 μM) for 24 h. Intracellular ROS in HepG2 cells and Hepa1–6 cells with or without PID1 overexpression upon treatment of three anticancer agents was detected by cytometry analysis and MFI was calculated. F-G Cell apoptosis in HepG2 cells and Hepa1–6 cells with or without PID1 overexpression upon treatment of three anticancer agents. H Cell apoptosis in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 24 h was examined by cytometry analysis. I Mitochondrial membrane potential in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 24 h was assessed by cytometry analysis and Red/Green ratio was calculated. J Intracellular ROS in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 24 h was assessed by cytometry analysis and MFI was calculated. K Cell viability curves of Hep3B cells with or without PID1 deficiency treated with the indicated doses of anticancer agents for 24 h. Data are expressed as mean ± SD (n = 3). *p < 0.05; **p < 0.01; ***p < 0.001.
