ArticleOncology letters2021
Identification of the molecular function of tripartite motif containing 58 in human lung cancer.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- SPRY domains encode ubiquitin ligase specificity for ZAP and RIG-I.PLoS pathogens · 2026Article
- Exploring the molecular function of LYPD3 from pan-cancer to lung cancer: based on bioinformatics and cellular experiments.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Multi-omics analysis of core E3 ubiquitin ligase identifies prognostic biomarkers associated with immune infiltration and drug sensitivity in lung adenocarcinoma.Journal of Cancer · 2025Article
- TRIM58 downregulation maintains stemness via MYH9-GRK3-YAP axis activation in triple-negative breast cancer stem cells.Cancer gene therapy · 2024Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
Lung cancer is a major public health problem worldwide, with a high associated incidence and mortality. In the present study, novel epigenetic signatures were identified through genome-wide DNA methylation microarrays. The results revealed that tripartite motif containing 58 (TRIM58), a potential tumor suppressor gene exhibited high methylation and low expression in lung cancer tissue samples compared with normal tissues. Receiver operating characteristic curve analysis demonstrated that TRIM58 may be a promising early diagnostic indicator of lung cancer. In addition, the present study analyzed the role of TRIM58 in tumorigenesis and development in lung cancer A549 cells. Wound healing assay and transwell migration assay were used to investigate cell migration, and flow cytometry analysis was used to detect apoptosis. Silencing TRIM58 accelerated the proliferation and migration of lung cancer cells. In contrast, the overexpression of TRIM58 significantly inhibited the proliferation and migration of lung cancer cells and promoted apoptosis. Gene set enrichment analysis revealed that TRIM58 expression was negatively correlated with MYC targets, G
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