Skip to main content
. 2024 May 28;31(7):881–896. doi: 10.1038/s41418-024-01310-9

Fig. 1. HSP70 inhibition impairs mitochondrial function and induces ROS.

Fig. 1

A–C Mitochondrial oxygen consumption rates (OCR) were measured in pancreatic cancer cell lines (PANC-1 and MIA PaCa-2), as well as non-transformed pancreatic ductal cells (hTERT-HPNE), in the presence or absence of 500 nM of HSP70i (AP-4-139B). All experiments were performed in triplicate, with each group containing 8–10 technical replicates. D–F Basal oxygen consumption rates (OCR), maximal respiration, and ATP production were analyzed and quantified in the presence or absence of 500 nM AP-4-139B. **p < 0.01, ***p < 0.001, n.s. not significant. G–H PANC-1 and MIA PaCa-2 cells were treated with the indicated doses of AP-4-139B for 48 h. Cells were then incubated with MitoSOX-Green, harvested, and analyzed by flow cytometry to determine mitochondrial ROS production. Fluorescence mean was analyzed and plotted on a histogram. *p < 0.05; n = 3 independent experiments. PANC-1 (I) and MIA PaCa-2 (J) cells were treated with the indicated doses of AP-4-139B for 24 h. Cells were then stained with 50 nM of TMRE for 30 min, and fluorescence intensity was measured using a plate reader. Shown are representative data of two independent experiments, with each condition containing six technical replicates. ***p < 0.001.