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The Expression Patterns of Human Cancer-Testis Genes Are Induced through Epigenetic Drugs in Colon Cancer Cells

Background: The expression of human germline genes is restricted to the germ cells of the gonads, which produce sperm and eggs. The germline genes involved in testis development and potentially activated in cancer cells are known as cancer-testis (CT) genes. These genes are potential therapeutic tar...

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Autores principales: Almutairi, Mikhlid H., Alrubie, Turki M., Almutairi, Bader O., Alamri, Abdullah M., Alrefaei, Abdulwahed F., Arafah, Maha M., Alanazi, Mohammad, Semlali, Abdelhabib
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9692864/
https://www.ncbi.nlm.nih.gov/pubmed/36355490
http://dx.doi.org/10.3390/ph15111319
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author Almutairi, Mikhlid H.
Alrubie, Turki M.
Almutairi, Bader O.
Alamri, Abdullah M.
Alrefaei, Abdulwahed F.
Arafah, Maha M.
Alanazi, Mohammad
Semlali, Abdelhabib
author_facet Almutairi, Mikhlid H.
Alrubie, Turki M.
Almutairi, Bader O.
Alamri, Abdullah M.
Alrefaei, Abdulwahed F.
Arafah, Maha M.
Alanazi, Mohammad
Semlali, Abdelhabib
author_sort Almutairi, Mikhlid H.
collection PubMed
description Background: The expression of human germline genes is restricted to the germ cells of the gonads, which produce sperm and eggs. The germline genes involved in testis development and potentially activated in cancer cells are known as cancer-testis (CT) genes. These genes are potential therapeutic targets and biomarkers, as well as drivers of the oncogenic process. CT genes can be reactivated by treatment with drugs that demethylate DNA. The majority of the existing literature on CT gene activation focuses on X-chromosome-produced CT genes. We tested the hypothesis that epigenetic landscape changes, such as DNA methylation, can alter several CT gene expression profiles in cancer and germ cells. Methods: Colon cancer (CC) cell lines were treated with the DNA methyltransferase inhibitor (DNMTi) 5-aza-2’-deoxycytidine, or with the histone deacetylase inhibitor (HDACi) trichostatin A (TSA). The effects of these epigenetic treatments on the transcriptional activation of previously published CT genes (CTAG1A, SCP2D1, TKTL2, LYZL6, TEX33, and ACTRT1) and testis-specific genes (NUTM1, ASB17, ZSWIM2, ADAM2, and C10orf82) were investigated. Results: We found that treatment of CC cell lines with 5-aza-2’-deoxycytidine or TSA correlated with activation of X-encoded CT genes and non-X-encoded CT genes in somatic (non-germline) cells. Conclusion: These findings confirm that a subset of CT genes can be regulated by hypomethylating drugs and subsequently provide a potential therapeutic target for cancer.
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spelling pubmed-96928642022-11-26 The Expression Patterns of Human Cancer-Testis Genes Are Induced through Epigenetic Drugs in Colon Cancer Cells Almutairi, Mikhlid H. Alrubie, Turki M. Almutairi, Bader O. Alamri, Abdullah M. Alrefaei, Abdulwahed F. Arafah, Maha M. Alanazi, Mohammad Semlali, Abdelhabib Pharmaceuticals (Basel) Article Background: The expression of human germline genes is restricted to the germ cells of the gonads, which produce sperm and eggs. The germline genes involved in testis development and potentially activated in cancer cells are known as cancer-testis (CT) genes. These genes are potential therapeutic targets and biomarkers, as well as drivers of the oncogenic process. CT genes can be reactivated by treatment with drugs that demethylate DNA. The majority of the existing literature on CT gene activation focuses on X-chromosome-produced CT genes. We tested the hypothesis that epigenetic landscape changes, such as DNA methylation, can alter several CT gene expression profiles in cancer and germ cells. Methods: Colon cancer (CC) cell lines were treated with the DNA methyltransferase inhibitor (DNMTi) 5-aza-2’-deoxycytidine, or with the histone deacetylase inhibitor (HDACi) trichostatin A (TSA). The effects of these epigenetic treatments on the transcriptional activation of previously published CT genes (CTAG1A, SCP2D1, TKTL2, LYZL6, TEX33, and ACTRT1) and testis-specific genes (NUTM1, ASB17, ZSWIM2, ADAM2, and C10orf82) were investigated. Results: We found that treatment of CC cell lines with 5-aza-2’-deoxycytidine or TSA correlated with activation of X-encoded CT genes and non-X-encoded CT genes in somatic (non-germline) cells. Conclusion: These findings confirm that a subset of CT genes can be regulated by hypomethylating drugs and subsequently provide a potential therapeutic target for cancer. MDPI 2022-10-26 /pmc/articles/PMC9692864/ /pubmed/36355490 http://dx.doi.org/10.3390/ph15111319 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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/).
spellingShingle Article
Almutairi, Mikhlid H.
Alrubie, Turki M.
Almutairi, Bader O.
Alamri, Abdullah M.
Alrefaei, Abdulwahed F.
Arafah, Maha M.
Alanazi, Mohammad
Semlali, Abdelhabib
The Expression Patterns of Human Cancer-Testis Genes Are Induced through Epigenetic Drugs in Colon Cancer Cells
title The Expression Patterns of Human Cancer-Testis Genes Are Induced through Epigenetic Drugs in Colon Cancer Cells
title_full The Expression Patterns of Human Cancer-Testis Genes Are Induced through Epigenetic Drugs in Colon Cancer Cells
title_fullStr The Expression Patterns of Human Cancer-Testis Genes Are Induced through Epigenetic Drugs in Colon Cancer Cells
title_full_unstemmed The Expression Patterns of Human Cancer-Testis Genes Are Induced through Epigenetic Drugs in Colon Cancer Cells
title_short The Expression Patterns of Human Cancer-Testis Genes Are Induced through Epigenetic Drugs in Colon Cancer Cells
title_sort expression patterns of human cancer-testis genes are induced through epigenetic drugs in colon cancer cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9692864/
https://www.ncbi.nlm.nih.gov/pubmed/36355490
http://dx.doi.org/10.3390/ph15111319
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