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Fig. 8 | BMC Cancer

Fig. 8

From: Mitochondrial DNA abnormalities provide mechanistic insight and predict reactive oxygen species-stimulating drug efficacy

Fig. 8

Proposed mechanism of functional OXPHOS mutation-mediated cell survival upon treatment with ROS-stimulating agents in cancer cells. The 3D-structures of OXPHOS complexes I-V with the nuclear-encoded subunits shown as ribbons (grey) and mitochondrial-encoded subunits shown as space filling model (yellow). Functional OXPHOS variations (red spheres) lead to the overproduction of ROS (blue) and mitochondrial dysfunction which in turn trigger cellular adaptation mechanisms by activating nuclear responses. In response to oxidative stress, nucleus (light purple) upregulates the transcription of genes responsible of mitochondrial biogenesis (e.g. PGC-1α, light orange) and mtDNA (open green circles) replication and transcription in order to compensate the mutated copies of mtDNA and avoid the over accumulation of ROS. The positive correlations between the total number of functional OXPHOS variations, ROS level, mtDNAcn and drug resistance observed in the present study indicate that oxidative stress could promote cancer cell survival via nucleus-mitochondria crosstalk

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