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Upregulation of Myc promotes the evasion of NK cell-mediated immunity through suppression of NKG2D ligands in K562 cells

c-Myc is a characteristic oncogene with dual functions in cell proliferation and apoptosis. Since the overexpression of the c-Myc proto-oncogene is a common event in the development and growth of various human types of cancer, the present study investigated whether oncogenic c-Myc can alter natural...

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Autores principales: Lee, Young-Shin, Heo, Woong, Son, Cheol-Hun, Kang, Chi-Dug, Park, You-Soo, Bae, Jaeho
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755160/
https://www.ncbi.nlm.nih.gov/pubmed/31432134
http://dx.doi.org/10.3892/mmr.2019.10583
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author Lee, Young-Shin
Heo, Woong
Son, Cheol-Hun
Kang, Chi-Dug
Park, You-Soo
Bae, Jaeho
author_facet Lee, Young-Shin
Heo, Woong
Son, Cheol-Hun
Kang, Chi-Dug
Park, You-Soo
Bae, Jaeho
author_sort Lee, Young-Shin
collection PubMed
description c-Myc is a characteristic oncogene with dual functions in cell proliferation and apoptosis. Since the overexpression of the c-Myc proto-oncogene is a common event in the development and growth of various human types of cancer, the present study investigated whether oncogenic c-Myc can alter natural killer (NK) cell-mediated immunity through the expression of associated genes, using PCR, western blotting and flow cytometry assays. Furthermore, whether c-Myc could influence the expression levels of natural killer group 2 member D (NKG2D) ligands, which are well known NK activation molecules, as well as NK cell-mediated immunity, was investigated. c-Myc was inhibited by 10058-F4 treatment and small interfering RNA transfection. Upregulation of c-Myc was achieved by transfection with a pCMV6-myc vector. The inhibition of c-Myc increased MHC class I polyeptide-related sequence B and UL16 binding protein 1 expressions among NKG2D ligands, and the overexpression of c-Myc suppressed the expression of all NKG2D ligands, except MHC class I polyeptide-related sequence A. Furthermore, the alteration of c-Myc activity altered the susceptibility of K562 cells to NK cells. These results suggested that the overexpression of c-Myc may contribute to the immune escape of cancer cells and cell proliferation. Combined treatment with NK-based cancer immunotherapy and inhibition of c-Myc may achieve improved therapeutic results.
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spelling pubmed-67551602019-09-25 Upregulation of Myc promotes the evasion of NK cell-mediated immunity through suppression of NKG2D ligands in K562 cells Lee, Young-Shin Heo, Woong Son, Cheol-Hun Kang, Chi-Dug Park, You-Soo Bae, Jaeho Mol Med Rep Articles c-Myc is a characteristic oncogene with dual functions in cell proliferation and apoptosis. Since the overexpression of the c-Myc proto-oncogene is a common event in the development and growth of various human types of cancer, the present study investigated whether oncogenic c-Myc can alter natural killer (NK) cell-mediated immunity through the expression of associated genes, using PCR, western blotting and flow cytometry assays. Furthermore, whether c-Myc could influence the expression levels of natural killer group 2 member D (NKG2D) ligands, which are well known NK activation molecules, as well as NK cell-mediated immunity, was investigated. c-Myc was inhibited by 10058-F4 treatment and small interfering RNA transfection. Upregulation of c-Myc was achieved by transfection with a pCMV6-myc vector. The inhibition of c-Myc increased MHC class I polyeptide-related sequence B and UL16 binding protein 1 expressions among NKG2D ligands, and the overexpression of c-Myc suppressed the expression of all NKG2D ligands, except MHC class I polyeptide-related sequence A. Furthermore, the alteration of c-Myc activity altered the susceptibility of K562 cells to NK cells. These results suggested that the overexpression of c-Myc may contribute to the immune escape of cancer cells and cell proliferation. Combined treatment with NK-based cancer immunotherapy and inhibition of c-Myc may achieve improved therapeutic results. D.A. Spandidos 2019-10 2019-08-09 /pmc/articles/PMC6755160/ /pubmed/31432134 http://dx.doi.org/10.3892/mmr.2019.10583 Text en Copyright: © Lee et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Lee, Young-Shin
Heo, Woong
Son, Cheol-Hun
Kang, Chi-Dug
Park, You-Soo
Bae, Jaeho
Upregulation of Myc promotes the evasion of NK cell-mediated immunity through suppression of NKG2D ligands in K562 cells
title Upregulation of Myc promotes the evasion of NK cell-mediated immunity through suppression of NKG2D ligands in K562 cells
title_full Upregulation of Myc promotes the evasion of NK cell-mediated immunity through suppression of NKG2D ligands in K562 cells
title_fullStr Upregulation of Myc promotes the evasion of NK cell-mediated immunity through suppression of NKG2D ligands in K562 cells
title_full_unstemmed Upregulation of Myc promotes the evasion of NK cell-mediated immunity through suppression of NKG2D ligands in K562 cells
title_short Upregulation of Myc promotes the evasion of NK cell-mediated immunity through suppression of NKG2D ligands in K562 cells
title_sort upregulation of myc promotes the evasion of nk cell-mediated immunity through suppression of nkg2d ligands in k562 cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755160/
https://www.ncbi.nlm.nih.gov/pubmed/31432134
http://dx.doi.org/10.3892/mmr.2019.10583
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