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. 2022 Jul 7;12:897703. doi: 10.3389/fonc.2022.897703

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Copyright © 2022 De Re, Rossetto, Rosignoli, Muraro, Racanelli, Tornesello, Zompicchiatti and Uzzau

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided tlammatory drugs ahe original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Non-steroidal anti-inflammatory drugs and anticancer drugs by inhibiting inflammation reduce the activation of the NF-kB signaling, resulting in the apoptosis cell death and the activation of the immune cell response. DRs, death receptors; NSAIDs, non-steroidal anti-inflammatory drugs; NF-kB, nuclear factor-kB; BCL-2, antiapoptotic B-cell lymphoma; Cyt c, cytochrome C. TNF-aR, Tumor necrosis factor receptor alfa; IL-1R, Interleukin-1 receptor; DAMPs, Damage-associated molecular patterns; TLR, Toll like receptor; NSAIDS, Non-steroidal anti-inflammatory drugs; COX-2, Cyclooxygenase-2; Mcl-1, Induced myeloid leukemia cell differentiation protein; ER, endoplasmic reticulum; Bcl-x, Apoptosis regulator Bcl-extra; IL-6, Interleukin 6.