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Uncovering BTB and CNC Homology1 (BACH1) as a Novel Cancer Therapeutic Target

BTB and CNC homology1 (BACH1), working as a transcriptional factor, is demonstrated to function on the regulation of epigenetic modifications by complex regulatory networks. Although BACH1 is reported as an oncogene, the overall analysis of its role remains lacking. In this study, we uncovered the c...

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Autores principales: Liu, Zheming, Wang, Jing, Chen, Huiyong, Wu, Zankai, Liao, Fuben, Wang, Sheng, Zhu, Ting
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9149251/
https://www.ncbi.nlm.nih.gov/pubmed/35651942
http://dx.doi.org/10.3389/fgene.2022.920911
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author Liu, Zheming
Wang, Jing
Chen, Huiyong
Wu, Zankai
Liao, Fuben
Wang, Sheng
Zhu, Ting
author_facet Liu, Zheming
Wang, Jing
Chen, Huiyong
Wu, Zankai
Liao, Fuben
Wang, Sheng
Zhu, Ting
author_sort Liu, Zheming
collection PubMed
description BTB and CNC homology1 (BACH1), working as a transcriptional factor, is demonstrated to function on the regulation of epigenetic modifications by complex regulatory networks. Although BACH1 is reported as an oncogene, the overall analysis of its role remains lacking. In this study, we uncovered the capacity of BACH1 as a new pan-cancer therapeutic target. We found that BACH1 is highly expressed in abundant cancers and correlated with the poor prognosis of most cancers. The mutation sites of BACH1 varied in different cancer types and correlated to patients’ prognoses. The tumor mutation burden (TMB) in four cancer species and up to six tumor infiltrated immune cells had a significant relevance with BACH1. The enrichment analysis showed that the BACH1-associated genes were significantly enriched in the pathways of PD-1/L1 expression, ubiquitin-mediated proteolysis, T cell receptor, Th17 cell differentiation. We then demonstrated that BACH1 is positively correlated with the expression of many candidate genes, incluing SRPK2, GCLM, SLC40A1, and HK2 but negatively correlated with the expression of KEAP1 and GAPDH. Overall, our data shed light on BACH1’s effect on latent utility in cancer targeting therapy.
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spelling pubmed-91492512022-05-31 Uncovering BTB and CNC Homology1 (BACH1) as a Novel Cancer Therapeutic Target Liu, Zheming Wang, Jing Chen, Huiyong Wu, Zankai Liao, Fuben Wang, Sheng Zhu, Ting Front Genet Genetics BTB and CNC homology1 (BACH1), working as a transcriptional factor, is demonstrated to function on the regulation of epigenetic modifications by complex regulatory networks. Although BACH1 is reported as an oncogene, the overall analysis of its role remains lacking. In this study, we uncovered the capacity of BACH1 as a new pan-cancer therapeutic target. We found that BACH1 is highly expressed in abundant cancers and correlated with the poor prognosis of most cancers. The mutation sites of BACH1 varied in different cancer types and correlated to patients’ prognoses. The tumor mutation burden (TMB) in four cancer species and up to six tumor infiltrated immune cells had a significant relevance with BACH1. The enrichment analysis showed that the BACH1-associated genes were significantly enriched in the pathways of PD-1/L1 expression, ubiquitin-mediated proteolysis, T cell receptor, Th17 cell differentiation. We then demonstrated that BACH1 is positively correlated with the expression of many candidate genes, incluing SRPK2, GCLM, SLC40A1, and HK2 but negatively correlated with the expression of KEAP1 and GAPDH. Overall, our data shed light on BACH1’s effect on latent utility in cancer targeting therapy. Frontiers Media S.A. 2022-05-16 /pmc/articles/PMC9149251/ /pubmed/35651942 http://dx.doi.org/10.3389/fgene.2022.920911 Text en Copyright © 2022 Liu, Wang, Chen, Wu, Liao, Wang and Zhu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Genetics
Liu, Zheming
Wang, Jing
Chen, Huiyong
Wu, Zankai
Liao, Fuben
Wang, Sheng
Zhu, Ting
Uncovering BTB and CNC Homology1 (BACH1) as a Novel Cancer Therapeutic Target
title Uncovering BTB and CNC Homology1 (BACH1) as a Novel Cancer Therapeutic Target
title_full Uncovering BTB and CNC Homology1 (BACH1) as a Novel Cancer Therapeutic Target
title_fullStr Uncovering BTB and CNC Homology1 (BACH1) as a Novel Cancer Therapeutic Target
title_full_unstemmed Uncovering BTB and CNC Homology1 (BACH1) as a Novel Cancer Therapeutic Target
title_short Uncovering BTB and CNC Homology1 (BACH1) as a Novel Cancer Therapeutic Target
title_sort uncovering btb and cnc homology1 (bach1) as a novel cancer therapeutic target
topic Genetics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9149251/
https://www.ncbi.nlm.nih.gov/pubmed/35651942
http://dx.doi.org/10.3389/fgene.2022.920911
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