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A prognosis marker MUC1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research

BACKGROUND: MUC1 is a type I transmembrane protein that plays an important role in tumor cell signal transduction. Although current studies have shown that MUC1 is upregulated in bladder cancer (BC), the specific mechanism is still unclear. METHODS: We performed expression analysis, gene set enrichm...

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Autores principales: Qing, Liangliang, Li, Qingchao, Yang, Yongjin, Xu, Wenbo, Dong, Zhilong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9309451/
https://www.ncbi.nlm.nih.gov/pubmed/35879749
http://dx.doi.org/10.1186/s12894-022-01067-8
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author Qing, Liangliang
Li, Qingchao
Yang, Yongjin
Xu, Wenbo
Dong, Zhilong
author_facet Qing, Liangliang
Li, Qingchao
Yang, Yongjin
Xu, Wenbo
Dong, Zhilong
author_sort Qing, Liangliang
collection PubMed
description BACKGROUND: MUC1 is a type I transmembrane protein that plays an important role in tumor cell signal transduction. Although current studies have shown that MUC1 is upregulated in bladder cancer (BC), the specific mechanism is still unclear. METHODS: We performed expression analysis, gene set enrichment analysis, survival analysis, immune infiltration analysis, drug sensitivity analysis, and metabolism-related gene expression analysis on TCGA-BLCA, GES31684 and GSE13507. RESULTS: The expression of MUC1 in the tumor and lymphatic metastasis positive samples was significantly increased. Genes related to MUC1 expression were significantly enriched in immune response, ribosomes, exosomes, and energy metabolism. The results of the immune infiltration analysis showed that M1 macrophages in BC with high MUC1 expression were significantly decreased. Expression of MUC1 increases drug resistance in BC patients. In addition, MUC1 increases glycolysis, glucose uptake, and lactate production by inducing metabolic reprogramming. CONCLUSION: MUC1 has a significant effect on the metabolism and immune cell infiltration of BC, which may be the cause of increased drug resistance, and can be used as a molecular target for the diagnosis and treatment of BC.
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spelling pubmed-93094512022-07-25 A prognosis marker MUC1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research Qing, Liangliang Li, Qingchao Yang, Yongjin Xu, Wenbo Dong, Zhilong BMC Urol Research BACKGROUND: MUC1 is a type I transmembrane protein that plays an important role in tumor cell signal transduction. Although current studies have shown that MUC1 is upregulated in bladder cancer (BC), the specific mechanism is still unclear. METHODS: We performed expression analysis, gene set enrichment analysis, survival analysis, immune infiltration analysis, drug sensitivity analysis, and metabolism-related gene expression analysis on TCGA-BLCA, GES31684 and GSE13507. RESULTS: The expression of MUC1 in the tumor and lymphatic metastasis positive samples was significantly increased. Genes related to MUC1 expression were significantly enriched in immune response, ribosomes, exosomes, and energy metabolism. The results of the immune infiltration analysis showed that M1 macrophages in BC with high MUC1 expression were significantly decreased. Expression of MUC1 increases drug resistance in BC patients. In addition, MUC1 increases glycolysis, glucose uptake, and lactate production by inducing metabolic reprogramming. CONCLUSION: MUC1 has a significant effect on the metabolism and immune cell infiltration of BC, which may be the cause of increased drug resistance, and can be used as a molecular target for the diagnosis and treatment of BC. BioMed Central 2022-07-25 /pmc/articles/PMC9309451/ /pubmed/35879749 http://dx.doi.org/10.1186/s12894-022-01067-8 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Qing, Liangliang
Li, Qingchao
Yang, Yongjin
Xu, Wenbo
Dong, Zhilong
A prognosis marker MUC1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research
title A prognosis marker MUC1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research
title_full A prognosis marker MUC1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research
title_fullStr A prognosis marker MUC1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research
title_full_unstemmed A prognosis marker MUC1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research
title_short A prognosis marker MUC1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research
title_sort prognosis marker muc1 correlates with metabolism and drug resistance in bladder cancer: a bioinformatics research
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9309451/
https://www.ncbi.nlm.nih.gov/pubmed/35879749
http://dx.doi.org/10.1186/s12894-022-01067-8
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