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Fig. 7 | Cancer & Metabolism

Fig. 7

From: Knockout of Vdac1 activates hypoxia-inducible factor through reactive oxygen species generation and induces tumor growth by promoting metabolic reprogramming and inflammation

Fig. 7

Schematic representation of the impact of Vdac1 knockout (Vdac1 −/−) on proliferation and cell death of MEF in vitro (a) and tumor growth in vivo (b). a In normoxia (Nx), the knockout of Vdac1 was associated with production of ROS that reduced proliferation and increased apoptosis (cytochrome C leakage). In hypoxia (Hx), the knockout of Vdac1 maintained the production of ROS but the effect was offset by inhibition of DUSP6 while allowing slight activation of P-ERK. Activated P-ERK effected the activity of COX7A1 and COX4-2, while promoting proliferation. b Through production of ROS, which stabilizes HIF-1α, a cascade of events induced (+) or repressed (−) processes that destabilized blood vessels and induced an inflammatory response. This cascade will then lead to a pro-tumoral response. αSMA: alpha-smooth muscle actin; THBD: thrombomodulin; CDKN2A: cyclin-dependent kinase inhibitor 2A; CxCL5: chemokine (C-X-C motif) ligand 5; IL8: interlukin 8; MMP3: matrix metallopeptidase 3

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Cancer & Metabolism

ISSN: 2049-3002