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. 2015 Feb 27;6(6):3947–3962. doi: 10.18632/oncotarget.2968

Figure 6. Mitochondrial dysfunction leads to increase of glycolysis activity and accumulation of NADH in T-Rex/293 cells.

Figure 6

(A–B) K-Ras activation and knockdown of NDUFAF1 caused increase of glycolytic activity as measured by glucose uptake and lactate production. Long, K-Ras induction for more than 1 month by addition of doxycycline. (C) Inhibitor of mitochondrial respiratory chain complex I by rotenone (10 nM) caused increase of glycolytic activity in TRex/293 cells. (D) Oxygen consumption remained inhibited after long term induction of K-Ras (>1 month). (E) ATP production remained unchanged after long term induction of K-Ras. (F–G) Activation of K-Ras for 24 h and knockdown of NDUFAF1 caused increase of NADH generation.