Fig. 3

Crosstalk between autophagy and inflammasome activation in cancer. The crosstalk between autophagy and inflammasome activation regulates multiple physiological and pathological responses, including cancer. Mitochondrial dysfunction and mitochondrial ROS generation can activate autophagy/mitophagy, as well as act as the second signal for inflammasome activation and pyroptosis. Dysfunctional autophagy results in excessive mitochondrial oxidative stress, leading to autophagic cell death, inflammasome activation, and pyroptosis. Elevated mitochondrial ROS levels can also promote oncogenesis, chemoresistance, and metastasis. Furthermore, mitochondria-associated membranes at the ER-mitochondria contact sites are signaling hubs for mitochondrial Ca²⁺ transfer from the ER to mitochondria through IP3R3s, mediating NLRP3 inflammasome activation in response to mitochondrial damage. IP3R3s are upregulated in various cancers