Fig. 8
From: Selective autophagy in cancer: mechanisms, therapeutic implications, and future perspectives
Mitophagy provides sufficient nutrition, energy and oxygen for cancer cells. The Warburg effect is the process by which glycolysis-a process that converts glucose into lactic acid-is promote by mitophagy. Mitochondrial OXPHOS and glycolysis act in concert to maintain the balance of energy metabolism in cancer cells. Parkin loss stimulates PTEN degradation, which in turn sets off the typical carcinogenic pathway known as PI3K/AKT signaling. This route expedites cancer cells’ aerobic glycolysis. Similarly, PINK1 absence can cause the Warburg effect by lowering Pyruvate kinase M2 (PKM2) activity and stabilizing HIF1a, which keeps cancer cells proliferating quickly. PKM2 is one of the key enzymes in glycolysis, and reducing PKM2 activity can promote the rapid proliferation of cancer cells by stimulating the pentose phosphate pathway. Moreover, hexokinase 2 (HK2) is selectively degraded by p62/SQSTM1-dependent mitophagy to control glycolysis levels. HIF1a transcription is up-regulated, initiating glycolytic metabolism, and its target genes are expressed more, which controls mitophagy. Hypoxia stimulation and the increase and elevation of mitochondrial ROS also cause these effects