BioMed Research International / 2021 / Article / Tab 2 / Review Article
Differences of Key Proteins between Apoptosis and Necroptosis Table 2 Necroptosis mechanism in cancer disease.
Protein Up/down Description Article related to necroptosis References TNF Up Tumor necrosis factor Fisetin significantly increases TNF and IK expression while decreasing pNF-, and pIK expression [35 ] RIPK1 and RIPK3 Up Receptor-interacting protein kinase-1 and 3 In the presence of ZVAD, MCF-7 cells express substantially more RIPK1 and RIPK3 in response to Que than in the absence of ZVAD [33 ] TNFR1 Up TNF’s receptor following the formation of two TNFR complexes Cell survival, apoptosis, or necroptosis can result from TNFR1 stimulation caused by damage, cellular stress, or infection [8 , 36 ] TNF-α , TNFR1, and necroptosis protein expression are all inhibited by PPO, indicating that PPO can protect neurons by preventing TNF-α -induced necroptosis [37 ] FADD Up Fas-associated protein with death domain (FADD). Activation of MLKL Necroptosis is caused by caspase-8, FADD, and RIPK3 (complex IIa/b) [36 ] FADD expression in HepG2 is reduced by fisetin treatment. FADD protects intestinal epithelial cells from RIP3-induced cell necrosis [35 ] MLKL Up MLKL (mixed lineage kinase like) after rapid plasma membrane rupture and inflammatory response via DAMP and cytokine release M1 CM significantly increases expression levels of MLKL, RIPK3, and p-MLKL after quercetin treatment [36 , 38 ]