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鉴定TRIM56作为肺腺癌的潜在生物标志物

Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma.

作者信息

Lu Kun, Sui Yingli, Fu Lin

机构信息

Institute of Chronic Disease, School of Basic Medicine, Qingdao University, Qingdao, Shandong, People's Republic of China.

出版信息

Cancer Manag Res. 2021 Mar 4;13:2201-2213. doi: 10.2147/CMAR.S288111. eCollection 2021.

DOI:10.2147/CMAR.S288111
PMID:33707970
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7940991/
Abstract

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.

摘要

背景

肺腺癌（LUAD）是人类肺癌的主要亚型。目前，LUAD患者的治疗效果和长期生存率并不理想。含三联基序蛋白56（TRIM56）是TRIM蛋白家族的成员，主要在免疫和癌症中发挥作用。

目的

研究TRIM56在LUAD中的表达情况，并探讨TRIM56对LUAD细胞侵袭和迁移的潜在调控作用。

方法

利用基因表达综合数据库和癌症基因组图谱-LUAD队列分析TRIM56在LUAD中的mRNA表达。从癌症基因组图谱-LUAD队列中获得与TRIM56相关的miRNA差异表达谱。进行基因本体论和京都基因与基因组百科全书通路富集分析，以确定miRNA和相互作用蛋白的主要功能。采用Transwell实验和伤口愈合实验检测TRIM56过表达对LUAD细胞侵袭和迁移的影响。

结果

TRIM56在LUAD中的表达降低，且与预后不良相关。我们确定了TRIM56的基因组拷贝数、负相关miRNA和潜在转录因子，并进行了富集分析。其中，hsa-mir-542和hsa-mir-627最有可能抑制TRIM56的表达。我们还预测了TRIM56的相互作用蛋白和潜在泛素化底物。最后，我们证明TRIM56过表达可抑制LUAD细胞的侵袭和迁移。

结论

本研究首次分析了TRIM56的表达及其对LUAD细胞侵袭和迁移的抑制作用。这一证据为进一步研究LUAD中TRIM56低表达的原因及其调控机制提供了新的方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/d2c8e33a6e73/CMAR-13-2201-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/59eb2bb527db/CMAR-13-2201-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/24f29e35acad/CMAR-13-2201-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/0dec56f0f470/CMAR-13-2201-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/8d857a4c61de/CMAR-13-2201-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/d2c8e33a6e73/CMAR-13-2201-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/59eb2bb527db/CMAR-13-2201-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/24f29e35acad/CMAR-13-2201-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/0dec56f0f470/CMAR-13-2201-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/8d857a4c61de/CMAR-13-2201-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/7940991/d2c8e33a6e73/CMAR-13-2201-g0005.jpg

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