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. 2022 Oct 3;13:960263. doi: 10.3389/fgene.2022.960263

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Copyright © 2022 Contreras-Sanzón, Prado-Garcia, Romero-Garcia, Nuñez-Corona, Ortiz-Quintero, Luna-Rivero, Martínez-Cruz and Carlos-Reyes.

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 the 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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The different states of chromatin are epigenetically regulated by HDACs and HDAC inhibitors, which determine the transcriptional activation or silencing of genes involved in lung cancer development. Studies from 2012 to 2021 showing the role of HDACs and HDAC inhibitors in the development of therapies against lung cancer. Created with biorender.com CSC, cigarette smoke condensate; iHDACs (MS-275, YCW1, SNOH-3, VPA = Valproic acid, TSA = Trichostatin A, SAHA = Vorinostat), Ac, acetylation.

Phosphorylation Acetylation Up-regulation Activation Inhibition Mechanism promoted by treatments

Inline graphic — The different states of chromatin are epigenetically regulated by HDACs and HDAC inhibitors, which determine the transcriptional activation or silencing of genes involved in lung cancer development. Studies from 2012 to 2021 showing the role of HDACs and HDAC inhibitors in the development of therapies against lung cancer. Created with biorender.com CSC, cigarette smoke condensate; iHDACs (MS-275, YCW1, SNOH-3, VPA = Valproic acid, TSA = Trichostatin A, SAHA = Vorinostat), Ac, acetylation.

Phosphorylation Acetylation Up-regulation Activation Inhibition Mechanism promoted by treatments