fig3

Dichloroacetate enhances the antitumor effect of pirarubicin via regulating the ROS-JNK signaling pathway in liver cancer cells

Figure 3. DCA increases THP-triggered ROS generation in liver cancer cells. A: Hep3B and Huh7 cells were treated with DCA (20 mmol/L), THP 300 nmol/L) or a combination of DCA and THP for 24 h. The cells were stained with a CM-H2DCFDA fluorescence probe, and the intensity of DCF fluorescence was measured by flow cytometry. The relative ROS change was presented as the fold change vs. the control group; B-D: Hep3B and Huh7 cells were treated with DCA combined with THP or DCA + THP + NAC (10 mmol/L) for 24 h. ROS level was then measured using the CM-H2DCFDA fluorescence probe (B), cell viability was measured using the CCK-8 assay (C) and apoptosis was determined by flow cytometry analysis (D). Data are presented as the mean ± SD from three independent experiments. *P < 0.05, **P < 0.01. DCA: dichloroacetate; THP: pirarubicin; ROS: reactive oxygen species

Cancer Drug Resistance
ISSN 2578-532X (Online)

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