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. 2017 Jun 21;22(6):1013. doi: 10.3390/molecules22061013

Figure 3.

Figure 3

A schematic representation of DET- and IDET-induced apoptosis in different cancer cell lines. DET and IDET trigger the activation of extrinsic apoptosis by activating caspase-8 which in turn either initiates the type 1 extrinsic apoptotic pathway by activating downstream effector caspase-3 or the type 2 extrinsic apoptotic pathway by truncation of Bid. DET and IDET induce intrinsic apoptosis by dissipating mitochondrial membrane potential and modulating the expression of Bcl-2 family proteins which results in the activation of caspase-3. Subsequently, activated caspase-3 leads to apoptosis by substrate cleavage. DET activates c-Jun N-terminal kinase (JNK) and p38 and inhibits the activation of Phosphatidylinositol-3-Kinase (PI3K)/AKT/ mammalian target of rapamycin (mTOR). DET inhibits the activation of extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinase (MAPK) and activates caspase-9 and induces apoptosis; ├ Inhibition, ↑ Up-regulation, ↓ Down-regulation.