PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications

<p>Tumor progression through immune evasion is a major challenge in cancer therapy. Recent studies revealed that enhanced PD-L1 expression in cancer stem cells is linked to immune evasion. Understanding the mechanisms behind this PD-L1 overexpression in cancer stem cells is critical for develo...

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Main Author: Pramod Darvin (153341) (author)
Other Authors: Varun Sasidharan Nair (5396393) (author), Eyad Elkord (14150214) (author)
Published: 2019
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author Pramod Darvin (153341)
author2 Varun Sasidharan Nair (5396393)
Eyad Elkord (14150214)
author2_role author
author
author_facet Pramod Darvin (153341)
Varun Sasidharan Nair (5396393)
Eyad Elkord (14150214)
author_role author
dc.creator.none.fl_str_mv Pramod Darvin (153341)
Varun Sasidharan Nair (5396393)
Eyad Elkord (14150214)
dc.date.none.fl_str_mv 2019-02-19T06:00:00Z
dc.identifier.none.fl_str_mv 10.1155/2019/3958908
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/PD-L1_Expression_in_Human_Breast_Cancer_Stem_Cells_Is_Epigenetically_Regulated_through_Posttranslational_Histone_Modifications/22082729
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biomedical and clinical sciences
Medical biotechnology
Oncology and carcinogenesis
Tumor
cancer therapy
stem cells
breast cancer cells
histone acetylation enzymes
dc.title.none.fl_str_mv PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p>Tumor progression through immune evasion is a major challenge in cancer therapy. Recent studies revealed that enhanced PD-L1 expression in cancer stem cells is linked to immune evasion. Understanding the mechanisms behind this PD-L1 overexpression in cancer stem cells is critical for developing more effective strategies for preventing immune evasion and increasing the efficacy of anti-PD-1/PD-L1 therapy. Tumorsphere formation in breast cancer cells enhanced epithelial to mesenchymal transition (EMT), which is evident by increased expression of mesenchymal markers. In this study, we analyzed CpG methylation of PD-L1 promoter in MCF-7 and BT-549 breast cancer cells and tumorspheres derived from them. PD-L1 promoter was significantly hypomethylated in MCF-7 tumorspheres, but not from BT-549 tumorspheres, compared with their cell line counterparts. The active demethylation of PD-L1 promoter was confirmed by the increase in the distribution of 5hmC and decrease in 5mC levels and the upregulation of TET3 and downregulation of DNMTs enzymes in MCF-7 tumorspheres, compared with the cell line. Additionally, we checked the distribution of repressive histones H3K9me3, H3K27me3, and active histone H3K4me3 in the PD-L1 promoter. We found that distribution of repressive histones to the PD-L1 promoter was lower in tumorspheres, compared with cell lines. Moreover, an overexpression of histone acetylation enzymes was observed in tumorspheres suggesting the active involvement of histone modifications in EMT-induced PD-L1 expression. In summary, EMT-associated overexpression of PD-L1 was partially independent of promoter CpG methylation and more likely to be dependent on posttranslational histone modifications. </p> <h2>Other information</h2> <p>Published in: Journal of Oncology<br> License: <a href="http://creativecommons.org/licenses/by/4.0" target="_blank">http://creativecommons.org/licenses/by/4.0</a><br> See article on publisher's website: <a href="http://dx.doi.org/10.1155/2019/3958908" target="_blank">http://dx.doi.org/10.1155/2019/3958908</a></p>
eu_rights_str_mv openAccess
id Manara2_1f8d05af6db7cc6cb55a03d6ff41e032
identifier_str_mv 10.1155/2019/3958908
network_acronym_str Manara2
network_name_str Manara2
oai_identifier_str oai:figshare.com:article/22082729
publishDate 2019
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spelling PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone ModificationsPramod Darvin (153341)Varun Sasidharan Nair (5396393)Eyad Elkord (14150214)Biomedical and clinical sciencesMedical biotechnologyOncology and carcinogenesisTumorcancer therapystem cellsbreast cancer cellshistone acetylation enzymes<p>Tumor progression through immune evasion is a major challenge in cancer therapy. Recent studies revealed that enhanced PD-L1 expression in cancer stem cells is linked to immune evasion. Understanding the mechanisms behind this PD-L1 overexpression in cancer stem cells is critical for developing more effective strategies for preventing immune evasion and increasing the efficacy of anti-PD-1/PD-L1 therapy. Tumorsphere formation in breast cancer cells enhanced epithelial to mesenchymal transition (EMT), which is evident by increased expression of mesenchymal markers. In this study, we analyzed CpG methylation of PD-L1 promoter in MCF-7 and BT-549 breast cancer cells and tumorspheres derived from them. PD-L1 promoter was significantly hypomethylated in MCF-7 tumorspheres, but not from BT-549 tumorspheres, compared with their cell line counterparts. The active demethylation of PD-L1 promoter was confirmed by the increase in the distribution of 5hmC and decrease in 5mC levels and the upregulation of TET3 and downregulation of DNMTs enzymes in MCF-7 tumorspheres, compared with the cell line. Additionally, we checked the distribution of repressive histones H3K9me3, H3K27me3, and active histone H3K4me3 in the PD-L1 promoter. We found that distribution of repressive histones to the PD-L1 promoter was lower in tumorspheres, compared with cell lines. Moreover, an overexpression of histone acetylation enzymes was observed in tumorspheres suggesting the active involvement of histone modifications in EMT-induced PD-L1 expression. In summary, EMT-associated overexpression of PD-L1 was partially independent of promoter CpG methylation and more likely to be dependent on posttranslational histone modifications. </p> <h2>Other information</h2> <p>Published in: Journal of Oncology<br> License: <a href="http://creativecommons.org/licenses/by/4.0" target="_blank">http://creativecommons.org/licenses/by/4.0</a><br> See article on publisher's website: <a href="http://dx.doi.org/10.1155/2019/3958908" target="_blank">http://dx.doi.org/10.1155/2019/3958908</a></p>2019-02-19T06:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1155/2019/3958908https://figshare.com/articles/journal_contribution/PD-L1_Expression_in_Human_Breast_Cancer_Stem_Cells_Is_Epigenetically_Regulated_through_Posttranslational_Histone_Modifications/22082729CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/220827292019-02-19T06:00:00Z
spellingShingle PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications
Pramod Darvin (153341)
Biomedical and clinical sciences
Medical biotechnology
Oncology and carcinogenesis
Tumor
cancer therapy
stem cells
breast cancer cells
histone acetylation enzymes
status_str publishedVersion
title PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications
title_full PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications
title_fullStr PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications
title_full_unstemmed PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications
title_short PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications
title_sort PD-L1 Expression in Human Breast Cancer Stem Cells Is Epigenetically Regulated through Posttranslational Histone Modifications
topic Biomedical and clinical sciences
Medical biotechnology
Oncology and carcinogenesis
Tumor
cancer therapy
stem cells
breast cancer cells
histone acetylation enzymes