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Differential Expression of Zinc-Dependent HDAC Subtypes and their Involvement in Unique Pathways Associated with Carcinogenesis
OBJECTIVE: The present study aims to identify the effect of ZnHDACs expression on the survival of the patients. Further, reveal the unique and common genes associated with each ZnHDACs and their associated pathways. METHODS: The patient data was obtained from the Cancer Genome Atlas Program (TCGA) d...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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West Asia Organization for Cancer Prevention
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9360949/ https://www.ncbi.nlm.nih.gov/pubmed/35345359 http://dx.doi.org/10.31557/APJCP.2022.23.3.877 |
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author | Ukey, Shweta Ramteke, Abhilash Choudhury, Chinmayee Purohit, Purvi Sharma, Praveen |
author_facet | Ukey, Shweta Ramteke, Abhilash Choudhury, Chinmayee Purohit, Purvi Sharma, Praveen |
author_sort | Ukey, Shweta |
collection | PubMed |
description | OBJECTIVE: The present study aims to identify the effect of ZnHDACs expression on the survival of the patients. Further, reveal the unique and common genes associated with each ZnHDACs and their associated pathways. METHODS: The patient data was obtained from the Cancer Genome Atlas Program (TCGA) database and was analyzed using cBioportal and Gene Expression Profiling Interactive Analysis 2(GEPIA2) online tools. Protein-protein interactions and functional interactomic analysis were done using STRING, DAVID, and KEGG pathway databases. RESULTS: HDAC1, 2, 8, 11 were over-expressed and, HDAC4, 5, 6, 7, and 10 were down-regulated in all the cancer types, but there are few exceptional expression patterns such as HDAC7 and HDAC10 overexpression in HNSC, HDAC3 down-regulation in LUAD, and PRAD. The unique genes interacting with each ZnHDACs provided a better understanding of ZnHDAC’s putative role in carcinogenesis. The present study reported that JARID2, stem cell regulation gene uniquely interacts with HDAC1, BPTF-CHRAC-BAZIA axis, enzymes for chromatin modeling selectively interacting with only HDAC2, HDAC3 in H2A acetylation via DMAP1 and YEATS4. HDAC6 associated unique genes regulate protein stability, HDAC7 in subnuclear localization and splicing, HDAC8 in telomere maintenance, HDAC9 in chromosomal rearrangements, and HDAC11 in maintaining histone core and folding. CONCLUSION: The unique genes and pathways associated with a particular ZnHDACs could provide a wide window for interrogating these genes for obtaining putative drug targets. |
format | Online Article Text |
id | pubmed-9360949 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | West Asia Organization for Cancer Prevention |
record_format | MEDLINE/PubMed |
spelling | pubmed-93609492022-08-10 Differential Expression of Zinc-Dependent HDAC Subtypes and their Involvement in Unique Pathways Associated with Carcinogenesis Ukey, Shweta Ramteke, Abhilash Choudhury, Chinmayee Purohit, Purvi Sharma, Praveen Asian Pac J Cancer Prev Research Article OBJECTIVE: The present study aims to identify the effect of ZnHDACs expression on the survival of the patients. Further, reveal the unique and common genes associated with each ZnHDACs and their associated pathways. METHODS: The patient data was obtained from the Cancer Genome Atlas Program (TCGA) database and was analyzed using cBioportal and Gene Expression Profiling Interactive Analysis 2(GEPIA2) online tools. Protein-protein interactions and functional interactomic analysis were done using STRING, DAVID, and KEGG pathway databases. RESULTS: HDAC1, 2, 8, 11 were over-expressed and, HDAC4, 5, 6, 7, and 10 were down-regulated in all the cancer types, but there are few exceptional expression patterns such as HDAC7 and HDAC10 overexpression in HNSC, HDAC3 down-regulation in LUAD, and PRAD. The unique genes interacting with each ZnHDACs provided a better understanding of ZnHDAC’s putative role in carcinogenesis. The present study reported that JARID2, stem cell regulation gene uniquely interacts with HDAC1, BPTF-CHRAC-BAZIA axis, enzymes for chromatin modeling selectively interacting with only HDAC2, HDAC3 in H2A acetylation via DMAP1 and YEATS4. HDAC6 associated unique genes regulate protein stability, HDAC7 in subnuclear localization and splicing, HDAC8 in telomere maintenance, HDAC9 in chromosomal rearrangements, and HDAC11 in maintaining histone core and folding. CONCLUSION: The unique genes and pathways associated with a particular ZnHDACs could provide a wide window for interrogating these genes for obtaining putative drug targets. West Asia Organization for Cancer Prevention 2022-03 /pmc/articles/PMC9360949/ /pubmed/35345359 http://dx.doi.org/10.31557/APJCP.2022.23.3.877 Text en https://creativecommons.org/licenses/by-nc/4.0/This work is licensed under a Creative Commons Attribution-Non Commercial 4.0 International License. https://creativecommons.org/licenses/by-nc/4.0/ |
spellingShingle | Research Article Ukey, Shweta Ramteke, Abhilash Choudhury, Chinmayee Purohit, Purvi Sharma, Praveen Differential Expression of Zinc-Dependent HDAC Subtypes and their Involvement in Unique Pathways Associated with Carcinogenesis |
title | Differential Expression of Zinc-Dependent HDAC Subtypes and their Involvement in Unique Pathways Associated with Carcinogenesis |
title_full | Differential Expression of Zinc-Dependent HDAC Subtypes and their Involvement in Unique Pathways Associated with Carcinogenesis |
title_fullStr | Differential Expression of Zinc-Dependent HDAC Subtypes and their Involvement in Unique Pathways Associated with Carcinogenesis |
title_full_unstemmed | Differential Expression of Zinc-Dependent HDAC Subtypes and their Involvement in Unique Pathways Associated with Carcinogenesis |
title_short | Differential Expression of Zinc-Dependent HDAC Subtypes and their Involvement in Unique Pathways Associated with Carcinogenesis |
title_sort | differential expression of zinc-dependent hdac subtypes and their involvement in unique pathways associated with carcinogenesis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9360949/ https://www.ncbi.nlm.nih.gov/pubmed/35345359 http://dx.doi.org/10.31557/APJCP.2022.23.3.877 |
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