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Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma

BACKGROUND: Lung adenocarcinoma (LUAD) is the primary subtype of human lung cancer. The effectiveness of treatment and long-term survival of patients with LUAD are current suboptimal. Tripartite motif containing 56 (TRIM56) is a member of the TRIM protein family that have functions predominantly in...

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Autores principales: Lu, Kun, Sui, Yingli, Fu, Lin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7940991/
https://www.ncbi.nlm.nih.gov/pubmed/33707970
http://dx.doi.org/10.2147/CMAR.S288111
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author Lu, Kun
Sui, Yingli
Fu, Lin
author_facet Lu, Kun
Sui, Yingli
Fu, Lin
author_sort Lu, Kun
collection PubMed
description BACKGROUND: Lung adenocarcinoma (LUAD) is the primary subtype of human lung cancer. The effectiveness of treatment and long-term survival of patients with LUAD are current suboptimal. Tripartite motif containing 56 (TRIM56) is a member of the TRIM protein family that have functions predominantly in immunity and cancer. PURPOSE: To investigate the expression of TRIM56 in LUAD, and explore the potential regulatory role of TRIM56 in the invasion and migration of LUAD cells. METHODS: The Gene Expression Omnibus datasets and The Cancer Genome Atlas-LUAD cohort were used to analyze the mRNA expression of TRIM56 in LUAD. The differential expression profiles of miRNAs associated with TRIM56 were obtained from The Cancer Genome Atlas-LUAD cohort. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to determine the principal functions of miRNAs and interacting proteins. Transwell and wound healing were used to detect the effect of overexpression of TRIM56 on the invasion and migration of LUAD cells. RESULTS: The expression of TRIM56 was decreased in LUAD and associated with poor prognosis. We determined the genome copy number, negatively correlated miRNA and potential transcription factors of TRIM56, and conducted enrichment analysis. Among them, hsa-mir-542 and hsa-mir-627 were the most likely to inhibit the expression of TRIM56. We also predicted the interacting proteins and potential ubiquitination substrate of TRIM56. Finally, we demonstrated that overexpression of TRIM56 inhibits the invasion and migration of LUAD cells. CONCLUSION: This study is the first to analyze the expression of TRIM56 and its inhibitory effect on the invasion and migration of LUAD. This evidence provides a new direction for further study of the reasons for the low expression of TRIM56 in LUAD and its regulatory mechanism.
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spelling pubmed-79409912021-03-10 Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma Lu, Kun Sui, Yingli Fu, Lin Cancer Manag Res Original Research BACKGROUND: Lung adenocarcinoma (LUAD) is the primary subtype of human lung cancer. The effectiveness of treatment and long-term survival of patients with LUAD are current suboptimal. Tripartite motif containing 56 (TRIM56) is a member of the TRIM protein family that have functions predominantly in immunity and cancer. PURPOSE: To investigate the expression of TRIM56 in LUAD, and explore the potential regulatory role of TRIM56 in the invasion and migration of LUAD cells. METHODS: The Gene Expression Omnibus datasets and The Cancer Genome Atlas-LUAD cohort were used to analyze the mRNA expression of TRIM56 in LUAD. The differential expression profiles of miRNAs associated with TRIM56 were obtained from The Cancer Genome Atlas-LUAD cohort. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to determine the principal functions of miRNAs and interacting proteins. Transwell and wound healing were used to detect the effect of overexpression of TRIM56 on the invasion and migration of LUAD cells. RESULTS: The expression of TRIM56 was decreased in LUAD and associated with poor prognosis. We determined the genome copy number, negatively correlated miRNA and potential transcription factors of TRIM56, and conducted enrichment analysis. Among them, hsa-mir-542 and hsa-mir-627 were the most likely to inhibit the expression of TRIM56. We also predicted the interacting proteins and potential ubiquitination substrate of TRIM56. Finally, we demonstrated that overexpression of TRIM56 inhibits the invasion and migration of LUAD cells. CONCLUSION: This study is the first to analyze the expression of TRIM56 and its inhibitory effect on the invasion and migration of LUAD. This evidence provides a new direction for further study of the reasons for the low expression of TRIM56 in LUAD and its regulatory mechanism. Dove 2021-03-04 /pmc/articles/PMC7940991/ /pubmed/33707970 http://dx.doi.org/10.2147/CMAR.S288111 Text en © 2021 Lu et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Lu, Kun
Sui, Yingli
Fu, Lin
Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma
title Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma
title_full Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma
title_fullStr Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma
title_full_unstemmed Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma
title_short Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma
title_sort identification of trim56 as a potential biomarker for lung adenocarcinoma
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7940991/
https://www.ncbi.nlm.nih.gov/pubmed/33707970
http://dx.doi.org/10.2147/CMAR.S288111
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