ArticleCell cycle (Georgetown, Tex.)2023
TRIM13 inhibits cell proliferation and induces autophagy in lung adenocarcinoma by regulating KEAP1/NRF2 pathway.
Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Integrated bioinformatics analyses and cell line experiments implicate miR-33a-5p/HIF1A in the cellular response to celastrol in lung adenocarcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Pan-cancer multi-omics analysis identifies SYNGR4 as a novel clinical prognostic biomarker and therapeutic target in lung adenocarcinoma.Discover oncology · 2026Article
- Post-translational modifications of selective autophagy receptors: orchestrating cellular homeostasis, disease pathogenesis, and therapeutic opportunities.Cellular & molecular biology letters · 2026Review
- Review
- Deubiquitinase TRIM44 Promotes Autophagy-Mediated Chemoresistance in Diffuse Large B Cell Lymphoma.Hematological oncology · 2025Article
- RBM15-dependent m6A modification mediates progression of non-small cell lung cancer cells.Molecular medicine (Cambridge, Mass.) · 2024Article
- Trim13-induced ubiquitination of RPS27A inhibits the progression of lung cancer by depending on the inactivation of NF-κB signaling pathway.Physiological reports · 2024Article
- Inhibition of ALKBH5 inhibits inflammation and excessive proliferation by promoting TRIM13 m6A modifications in glomerular mesangial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins.Cellular & molecular biology letters · 2024Review
- Nrf2 in human cancers: biological significance and therapeutic potential.American journal of cancer research · 2024Review
- Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) is the most common type of lung cancer. Tripartite motif 13 (TRIM13) is a member of TRIM protein family and is downregulated in multiple cancers, especially non-small cell lung cancers (NSCLC). In this study, we investigated anti-tumor mechanism of TRIM13 in non-small cell lung cancer tissues and cell lines. First, the mRNA and protein levels of TRIM13 in LUAD tissue and cells were measured. TRIM13 was overexpressed on LUAD cells to investigate the effects on cell proliferation, apoptosis, oxidative stress, p62 ubiquitination, and autophagy activation. Finally, mechanistic role of TRIM13 in regulating the Keap1/Nrf2 pathway was investigated. Results indicated that low level of TRIM13 mRNA and protein expression was found in LUAD tissue and cells. Overexpression of TRIM13 in LUAD cancer cells suppressed their proliferation, increased apoptosis, and oxidative stress, ubiquitinated p62, and activated autophagy via the RING finger domain of TRIM13. Furthermore, TRIM13 showed interaction with p62 and mediated its ubiquitination and degradation in LUAD cells. Mechanistically, TRIM13 exerted the tumor suppressor functions in LUAD cells by negatively regulating Nrf2 signaling and downstream antioxidants, which was further confirmed by in vivo data from xenografts. In conclusion, TRIM13 behaves like a tumor suppressor and triggers autophagy in LUAD cells by mediating p62 ubiquitination via KEAP1/Nrf2 pathway. Our findings provide a novel insight into targeted therapy plans for LUAD.
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