Fig. 3
Disturbance in PDAC mitochondrial network dynamics leads to poor response to initial extracellular acidotic stress. a SUIT-2 PDAC cells under different control and acidic stress conditions (Ctrl, S.A., & L.A.) were individually transfected with the control HA-tagged plasmid, the phosphodeficient DRP1S637A mutant, or the phosphomimetic DRP1S637D variant. MTT proliferation assays (mean ± SD, n = 3, fold-change relative to day 1) and Western blot analyses were performed to assess the impact of altered DRP1 fission activity in disrupting mitochondrial network dynamics involved in the early response and late adaptation to acidic pHe stress. b The same three SUIT-2 PDAC cell groups (Ctrl, S.A., & L.A.) were individually transfected with either negative control non-targeting siRNAs (siRNA-N.C.) or siRNAs against MFN2 (siRNA-MFN2). Tumor cells from each group without siRNA transfection served as null controls. The mean proliferation of each cell group was determined by MTT assays (mean ± SD, n = 3, fold-change relative to day 1), and the expression changes in mitophagy- and apoptosis-related molecules were determined by Western blot analyses; β-actin was the loading control