Journal: Molecules

Article Title: Apoptosis Induced by (−)-Epicatechin in Human Breast Cancer Cells is Mediated by Reactive Oxygen Species

doi: 10.3390/molecules25051020

Figure Lengend Snippet: Schematic representation of (−)-epicatechin anticancer activity in MDA-MB-231 and MCF-7 cells. The anticancer effect in MDA-MB-231 cells was possibly triggered through TRAIL receptor interaction (DR4/DR5) and its upregulation. This extrinsic pathway activation was enhanced through the intrinsic pathway, resulting in caspases-dependent apoptosis and enhanced by the modulating of inhibitors of apoptosis by Smac/Diablo and HtrA2/Omi (continuous arrow). In MCF-7 cells, an anticancer effect was evident through the interaction with another receptor, the modulation of cellular kinases, and the upregulation of pro-apoptotic proteins such as Bad and Bax. This Bad and Bax upregulation induced the leak of cytochrome C, Smac/Diablo, and HtrA2/Omi into the cytoplasm, activating apoptosis through the intrinsic pathway. These mechanisms are tightly related to ROS generation (dashes arrow). (Arrows indicate activation, ⊥ indicates inhibition).

Article Snippet: As shown in , in MDA-MB-231 cells treated with (−)-epicatechin’s IC 50 value concentration, an increase was generated in the expression of the proteins as follows (compare A with B): TRAIL receptors (R1/DR4, R2/DR5) (C1–C2, C3–C4), pro-caspase 3 (line B9–B10), SMAC/Diablo (line D15–D16), and HTRA2/Omi (lines C21–C22).

Techniques: Activity Assay, Activation Assay, Inhibition