Fig. 1

Core molecular mechanism of apoptosis, autophagy, ferroptosis, mitotic catastrophe, necroptosis, and anoikis. a There are two well-known signal transduction cascades regulating cell apoptosis: the extrinsic and intrinsic pathways. The extrinsic pathway is activated by death receptors and death ligands, while the intrinsic pathway is initiated by cellular stress-mediated mitochondria dysfunction. b The formation of the autophagosome depends on the formation of a complex incorporating Beclin-1, which is regulated by mTOR. Moreover, various proteins and signaling molecules (AMPK, PI3K, p62, etc.) are involved in the regulation of autophagy. c Ferroptosis is a type of regulated cell death that is induced by the iron-dependent accumulation of lipid reactive oxygen species (ROS) and lipid peroxidation, the inhibition of cystine/glutamate antiporter, and the loss of activity of glutathione peroxidase 4 (GPX4). d The cyclin-dependent kinase 1 (CDK1)/cyclin B1 complex is an important component of mitotic catastrophe and can promote cell cycle transition from G2 phase to M phase. Deoxyribonucleic acid (DNA) damage, mitotic defects, and cytokinesis failure are the three key factors leading to mitotic catastrophes. e Necroptosis is a form of regulated necrotic cell death stimulated by tumor necrosis factor-α (TNF-α). After TNFα binds to the receptor, tumor necrosis factor receptor 1 (TNFR1) recruits TNFRSF1A associated via death domain (TRADD), Fas associated via death domain (FADD), receptor-interacting serine/threonine kinase protein (RIPK) 1, TNF receptor-associated factor 2 (TRAF2) and other proteins to form complex I, and then RIPK1 is deubiquitinated to promote the transformation of complex I to complex II. When caspase-8 is inhibited, mixed lineage kinase domain-like protein (MLKL), RIPK1, and RIPK3 are recruited to form necrosome through phosphorylation, which eventually triggers necroptosis. f Anoikis induces cell death through conventional apoptotic pathways. B cell lymphoma 2 (Bcl-2) related proteins are widely involved in anoikis regulation, and multiple protein kinases are involved in the signal transduction of anoikis. When cells detach from the extracellular matrix (ECM), pro-survival signals cannot be activated, but the death receptors and mitochondrial apoptotic pathways are activated to prevent adherent-independent cell growth and attachment, and finally activate anoikis to induce cell death