ArticleScientific reports2017
TRIM14 is a Putative Tumor Suppressor and Regulator of Innate Immune Response in Non-Small Cell Lung Cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Whole-Genome Sequencing Reveals Breed-Specific SNPs, Indels, and Signatures of Selection in Royal White and White Dorper Sheep.Animals : an open access journal from MDPI · 2026Article
- Prediction of Prostate Adenocarcinoma Recurrence Prognosis and Immune Status Through 6-Acetoxy-Anopterine Resistance-Associated Programmed Cell Death Genes.Cancer management and research · 2026Article
- The TRIM14-KIF1B Axis Drives Renal Injury in Diabetic Nephropathy Through TLR4/NF-κB Pathway Modulation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Emerging discoveries on the role of TRIM14: from diseases to immune regulation.Cell death discovery · 2024Review
- Tripartite motif‑containing 14 may aggravate cardiac hypertrophy via the AKT signalling pathway in neonatal rat cardiomyocytes and transgenic mice.Molecular medicine reports · 2023Article
- Higher cytotoxic activities of CD8BMC immunology · 2023Article
- 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
- Article
- miR-671-5p repressed progression of papillary thyroid carcinoma via TRIM14.The Kaohsiung journal of medical sciences · 2021Article
- Article
- Therapeutic Targeting of Nemo-like Kinase in Primary and Acquired Endocrine-resistant Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- LncRNA MSC-AS1 Promotes Colorectal Cancer Progression by Regulating miR-325/TRIM14 Axis.Journal of oncology · 2021Article
- The Emerging Roles of Tripartite Motif Proteins (TRIMs) in Acute Lung Injury.Journal of immunology research · 2021Review
- lncRNA RPPH1 promotes non-small cell lung cancer progression through the miR-326/WNT2B axis.Oncology letters · 2020Article
- Therapeutic role of recurrent ESR1-CCDC170 gene fusions in breast cancer endocrine resistance.Breast cancer research : BCR · 2020Article
- TRIM14 promotes endothelial activation via activating NF-κB signaling pathway.Journal of molecular cell biology · 2020Article
- Article
- Somatic Alteration Burden Involving Non-Cancer Genes Predicts Prognosis in Early-Stage Non-Small Cell Lung Cancer.Cancers · 2019Article
- Tripartite motif-containing 14 (TRIM14) promotes epithelial-mesenchymal transition via ZEB2 in glioblastoma cells.Journal of experimental & clinical cancer research : CR · 2019Article
- TRIM14 promotes cell proliferation and inhibits apoptosis by suppressing PTEN in colorectal cancer.Cancer management and research · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small-cell lung carcinoma (NSCLC) accounts for 85% of malignant lung tumors and is the leading cause of cancer deaths. Our group previously identified Tripartite Motif 14 (TRIM14) as a component of a prognostic multigene expression signature for NSCLC. Little is known about the function of TRIM14 protein in normal or disease states. We investigated the functional and prognostic role of TRIM14 in NSCLC using in vitro and in vivo perturbation model systems. Firstly, a pooled RNAi screen identified TRIM14 to effect cell proliferation/survival in NSCLC cells. Secondly, silencing of TRIM14 expression significantly enhanced tumor growth in NSCLC xenograft mouse models, while exogenous TRIM14 expression attenuated tumorigenesis. In addition, differences in apoptotic activity between TRIM14-deficient and control tumors suggests that TRIM14 tumor suppressor activity may depend on cell death signaling pathways. TRIM14-deficient cell lines showed both resistance to hypoxia-induced cell death and attenuation of interferon response via STAT1 signaling. Consistent with these phenotypes, multivariate analyses on published mRNA expression datasets of over 600 primary NSCLCs demonstrated that low TRIM14 mRNA levels are significantly associated with poorer prognosis in early stage NSCLC patients. Our functional data therefore establish a novel tumor suppressive role for TRIM14 in NSCLC progression.
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