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. 2019 Aug 22;4(16):e126915. doi: 10.1172/jci.insight.126915

Figure 6. Patient-derived pancreatic cancer cells respond to leflunomide in a Kras-dependent fashion.

Figure 6

(A) Kras WT patient samples of PDAC exhibited elongated mitochondria similar to HPNE cells, while Kras mutant patient samples appeared punctate and fragmented. The mitochondria morphology from each genotype was quantified; n = 100–200. Quantification for intermediate and tubular mitochondrial morphology can be found in Supplemental Figure 6, B and C. (B) Leflunomide treatment on Kras mutant MDA-PATC53 cell line induces mitochondrial fusion, with quantification; n = 100–200 cells. *P = 0.02 for tubular, **P = 0.002 for fragmented by unpaired t test. (C) Mito Stress assay of MDA-PATC53 cells treated with 50 μM leflunomide, with quantification in D. *P = 0.04 by unpaired t test for basal and ATP production. Original magnification, ×60; scale bars: 10 μm. Data are presented as mean  ±  SEM. (E) Leflunomide treatment does not affect morphology in Kras WT MDA-PATC153 cell line, with quantification; n = 100–200 cells. (F) Mito Stress assay of MDA-PATC153 cells treated with 50 μM leflunomide, with quantification in G. Statistical analysis by unpaired t test. Data are presented as mean  ±  SEM.