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. 2019 Jul 2;20(13):3254. doi: 10.3390/ijms20133254

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Possible mode of cell death pathway in Caco-2 cells. Red arrows show either up- or down-regulated genes. Tumor necrosis factor receptor (TNFR) was up-regulated, signaling its proactive role in the receptor induced pathway and involvement of Caspases that precede apoptotic nuclear damage. TP53 (p53) activates pro-apoptotic genes (BAK and BIK), resulting in decreased mitochondrial membrane potential (MMP) and subsequent release of mitochondrial apoptotic contents such as cytochrome C (Cyto C) and direct IAP binding protein with low pI (DIABLO). DIABLO deactivates inhibitors of apoptosis proteins (IAPs) in order to potentiate apoptosis. Up-regulated CD27 and PYCARD are suggestive of an inflammatory response; however, NF_Kβ1 was neither up- nor down-regulated in Caco-2 cells, hence the uncertainty (?) regarding the involvement of inflammasomes.