Mitochondrial reorganization induces a metabolic shift to glycolysis. SH-EP/Ctr, SH-EP/Surv, and SH-EP/shSurv cells were treated with 20 µM LCL161 (A) or 24 µM TL32711 (B) for 24 hours. Cytoplasmic and mitochondrial extracts were analyzed for expression of mitochondrial respiration complexes I, II and IV (OXPHOS) as well as DRP1. CoxIV (mitochondrial) and α-Tubulin (cytoplasmic) served as markers for extract purity. Glucose consumption (C) and lactate production (D) was monitored after 72 hours treatment with low-dose LCL161 (5 µM) or TL32711 (3 µM). Untreated cells were set as 100%. Shown is the mean+SD of three independent experiments. Statistical differences between untreated and treated cells (***P<0.001, **P<0.01) or knock-down and control cells (### P<0.001, ##P<0.01, #P<0.05) were assessed by unpaired t-test. (E) Mitochondrial respiration was analyzed in SH-EP cells treated with 5 µM LCL161 for 72 hours using MitoStress Kit (Agilent, Santa Clara, USA) in a Seahorse XFp. SH-EP/Surv cells were used as control. Shown is the mean±SD of four independent experiments. Statistical differences to SH-EP/Ctr cells (***P<0.001, **P<0.01, *P<0.05)