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Fig. 2 | Molecular Cancer

Fig. 2

From: Crosstalk between metabolism and cell death in tumorigenesis

Fig. 2

Metabolites, metabolic pathways and related metabolic genes that take part in necrosis and necroptosis. Glucose starvation promotes necrosis through the transcription factor ATF4. In addition, it can act on p53, which regulates necroptosis by affecting the interaction between TRINGS and STRAP. Glucose deprivation also facilitates necroptosis by promoting the binding of mitochondrial DNA and ZBP1 to regulate MLKL, a key substance in the development of necroptosis. DHA supplementation with docetaxel (TXT) promotes necroptosis. As one of the key components of the necrosome that promotes the onset of necroptosis, MLKL function can be facilitated by GLTP. Very long chain saturated fatty acids participate in necroptosis by targeting MLKL. DMF promotes necroptosis by promoting the depletion of GSH, ROS generation and MAPK activation. The red boxes represent negative regulators and the green boxes represent positive regulators

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