ArticleCancer management and research2021
Identification of TRIM56 as a Potential Biomarker for Lung Adenocarcinoma.
Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- The oncogenic role of TRIM56 in pancreatic cancer via the TRAF6/NF-kB axis.Journal of molecular histology · 2025Article
- Article
- Review
- The Functions of TRIM56 in Antiviral Innate Immunity and Tumorigenesis.International journal of molecular sciences · 2023Review
- TRIM56 acts through the IQGAP1-CDC42 signaling axis to promote glioma cell migration and invasion.Cell death & disease · 2023Article
- TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein.Journal of experimental & clinical cancer research : CR · 2022Article
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- The TRIM proteins in cancer: from expression to emerging regulatory mechanisms.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- NMU Is a Poor Prognostic Biomarker in Patients with Lung Adenocarcinoma.Disease markers · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung 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.
methodsThe 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.
resultsThe 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.
conclusionThis 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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