Skip to main content
. Author manuscript; available in PMC: 2024 Jun 5.
Published in final edited form as: Nat Cancer. 2023 Jun 5;4(6):795–806. doi: 10.1038/s43018-023-00571-6

Figure 4: Non-lethal outcomes for apoptosis flatliners.

Figure 4:

Illustration of evident consequences of the sublethal engagement of the intrinsic pathway of apoptosis and their main molecular players. The release of PGE2 relays inhibitory effects on T cells and dendritic cells. PGE2 can promote a pro-proliferative state and cell survival. NF-κB engages pro-survival signaling. Sublethal cytochrome c release can activate the ISR and thereby ATF4 translation. ATF4 impacts on various signaling pathways that lead to an escape from cell death, an increased sensitivity towards ferroptosis and a metastatic phenotype. Latter can also be promoted by sublethal caspase activation followed by subsequent initiation of the JNK-AP1 pathway. ROS and CAD can cause DNA damage, leading to genome instability and mutation. The cytosolic release of mtDNA can activate the cGAS-STING pathway, which promotes senescence and a senescence-associated secretory phenotype (SASP).