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Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma

Authors Lu K, Sui Y, Fu L

Received 28 October 2020

Accepted for publication 17 February 2021

Published 4 March 2021 Volume 2021:13 Pages 2201—2213

DOI https://doi.org/10.2147/CMAR.S288111

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Harikrishna Nakshatri


Kun Lu, Yingli Sui, Lin Fu

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

Correspondence: Lin Fu
Institute of Chronic Disease, School of Basic Medicine, Qingdao University, No. 308 Ningxia Road, Qingdao City, Shandong Province, 266071, People’s Republic of China
Tel +86 138 1804 8288
Fax +86 532-85953085
Email [email protected]

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.

Keywords: TRIM56, lung adenocarcinoma, bioinformatics analysis, invasion, migration

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