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. 2021 Jun 28;26(13):3952. doi: 10.3390/molecules26133952

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© 2021 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 (https://creativecommons.org/licenses/by/4.0/).

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Altered transcription of NKG2D ligands after treatment with HDAC inhibitors. The transcription of NKG2D ligands was analyzed in lung cancer cells using multiplex RT-PCR. The NCI-H23 cells were each treated with 1, 10, 100, and 1000 nM of the following selective HDAC inhibitors: (A) FK228, (B) RGFP966, (C) MC1568, (D) Tubacin, and (E) PCI34051 for 18 h. (F) The A549 cells were treated with FK228 for 18 h. PCR products were separated and quantified using MultiNA. All experiments were performed in triplicate. Changes in transcription were normalized to the β-actin (ACTB) and presented as the mean fold change in comparison to the controls (treated with same amount of solvent, DMSO). * represents an increase, and # represents a decrease that has statistical significance. p-values less than 0.05, 0.01, and 0.001 are marked as */#, **/##, and ***, respectively.

Altered transcription of NKG2D ligands after treatment with HDAC inhibitors. The transcription of NKG2D ligands was analyzed in lung cancer cells using multiplex RT-PCR. The NCI-H23 cells were each treated with 1, 10, 100, and 1000 nM of the following selective HDAC inhibitors: (A) FK228, (B) RGFP966, (C) MC1568, (D) Tubacin, and (E) PCI34051 for 18 h. (F) The A549 cells were treated with FK228 for 18 h. PCR products were separated and quantified using MultiNA. All experiments were performed in triplicate. Changes in transcription were normalized to the β-actin (ACTB) and presented as the mean fold change in comparison to the controls (treated with same amount of solvent, DMSO). * represents an increase, and # represents a decrease that has statistical significance. p-values less than 0.05, 0.01, and 0.001 are marked as */#, **/##, and ***, respectively.