Fig. 6: Model of HSD-induced tumor growth suppression. | Cell Death & Disease

Fig. 6: Model of HSD-induced tumor growth suppression.

From: High-salt diet induces immune-independent re-differentiation, metabolic shut down and cell cycle arrest of melanoma

Fig. 6

During both, NSD and HSD nutrients are available and taken up by tumor cells. During NSD, MITF- as well as TSC2-levels are low, allowing mTORC1 signaling. This results in enhanced proteins synthesis, metabolic activity and progression through the cell cycle, while autophagy and melanogenesis remain on a basal level. Upon HSD, MITF and TSC2 are upregulated. ß-catenin acts as a co-factor that stabilizes MITF expression, resulting in increased melanogenesis. Due to high TSC2 activity, mTORC1 is downregulated, resulting in shutdown of metabolic activity and protein synthesis as well as cell cycle arrest (p18), accompanied by an increase in autophagy. Red arrows = inhibition; black arrows = induction; black, dashed arrows = proposed/hypothesized activation.

Back to article page