Fig. 7: Proposed model for P2Et effect on B16-F10 tumor cells. | Cell Death Discovery

Fig. 7: Proposed model for P2Et effect on B16-F10 tumor cells.

From: Polyphenol-rich extract induces apoptosis with immunogenic markers in melanoma cells through the ER stress-associated kinase PERK

Fig. 7: Proposed model for P2Et effect on B16-F10 tumor cells.The alternative text for this image may have been generated using AI.

a Inducers type I as doxorubicin induces DNA damage and ROS production, therefore, increase ER stress and autophagy associated with Ecto-CRT and ATP release, respectively. In addition, apoptosis is independent of PERK. b Inducers type II as Hyp-PDT increase ROS in ER and induce Ecto-CRT, ATP release and apoptosis in a PERK-dependent manner. In both types of ICD inducers, CRT exposure is dependent on ER-calcium levels depletion. c On the other hand, P2Et increase ER stress signaling via PERK promoting an increase in ER and cytoplasmic Ca2+ levels. This calcium will be in part responsible for the induction of mitochondrial damage and apoptosis without ROS participation. Parallel, P2Et also induced the ICD markers Ecto-CRT, and HMGB1 and ATP release in a PERK-dependent manner. Image created using BioRender (https://biorender.com/)

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