ArticleOncotarget2014
TRIM16 inhibits proliferation and migration through regulation of interferon beta 1 in melanoma cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
The trial behind it
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- TRIM16: a context-dependent E3 ligase in autophagy, oxidative stress, and immune regulation - from cancer and systemic disease.Frontiers in oncology · 2026Review
- Epigenetics of Malignant Melanoma: Mechanisms, Diagnostic Approaches and Therapeutic Applications.Oncology research · 2026Review
- TRIM16 Inhibits Inflammation by Interacting With and Ubiquitinating TRAF2 in a Colitis Model.Journal of cellular and molecular medicine · 2025Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- Bona Fide Tumor Suppressor Genes Hypermethylated in Melanoma: A Narrative Review.International journal of molecular sciences · 2021Review
- Withaferin A-A Promising Phytochemical Compound with Multiple Results in Dermatological Diseases.Molecules (Basel, Switzerland) · 2021Review
- Stromal Cells Present in the Melanoma Niche Affect Tumor Invasiveness and Its Resistance to Therapy.International journal of molecular sciences · 2021Review
- Withaferin A activates TRIM16 for its anti-cancer activity in melanoma.Scientific reports · 2020Article
- AKT-induced lncRNA VAL promotes EMT-independent metastasis through diminishing Trim16-dependent Vimentin degradation.Nature communications · 2020Article
- The Tripartite Nexus: Autophagy, Cancer, and Tripartite Motif-Containing Protein Family Members.Frontiers in pharmacology · 2020Review
- Long non-coding RNA CASC2 induces apoptosis and autophagy in human colon cancer cells via modulation of TRIM16 expression.American journal of translational research · 2020Article
- TRIM proteins in neuroblastoma.Bioscience reports · 2019Review
- Heterozygous loss of keratinocyte TRIM16 expression increases melanocytic cell lesions and lymph node metastasis.Journal of cancer research and clinical oncology · 2019Article
- Transcription factors Brn-3α and TRIM16 in cancers, association with hormone reception.Heliyon · 2019Review
- TRIM14 Promotes Breast Cancer Cell Proliferation by Inhibiting Apoptosis.Oncology research · 2019Article
- IL-32 gamma reduces lung tumor development through upregulation of TIMP-3 overexpression and hypomethylation.Cell death & disease · 2018Article
- TRIM56 Suppresses Multiple Myeloma Progression by Activating TLR3/TRIF Signaling.Yonsei medical journal · 2018Article
- Tripartite Motif 16 Inhibits the Migration and Invasion in Ovarian Cancer Cells.Oncology research · 2017Article
- TRIM16 suppresses the progression of prostate tumors by inhibiting the Snail signaling pathway.International journal of molecular medicine · 2016Article
- TRIMs and Galectins Globally Cooperate and TRIM16 and Galectin-3 Co-direct Autophagy in Endomembrane Damage Homeostasis.Developmental cell · 2016Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High basal or induced expression of the tripartite motif protein, TRIM16, leads to reduce cell growth and migration of neuroblastoma and skin squamous cell carcinoma cells. However, the role of TRIM16 in melanoma is currently unknown. TRIM16 protein levels were markedly reduced in human melanoma cell lines, compared with normal human epidermal melanocytes due to both DNA methylation and reduced protein stability. TRIM16 knockdown strongly increased cell migration in normal human epidermal melanocytes, while TRIM16 overexpression reduced cell migration and proliferation of melanoma cells in an interferon beta 1 (IFNβ1)-dependent manner. Chromatin immunoprecipitation assays revealed TRIM16 directly bound the IFNβ1 gene promoter. Low level TRIM16 expression in 91 melanoma patient samples, strongly correlated with lymph node metastasis, and, predicted poor patient prognosis in a separate cohort of 170 melanoma patients with lymph node metastasis. The BRAF inhibitor, vemurafenib, increased TRIM16 protein levels in melanoma cells in vitro, and induced growth arrest in BRAF-mutant melanoma cells in a TRIM16-dependent manner. High levels of TRIM16 in melanoma tissues from patients treated with Vemurafenib correlated with clinical response. Our data, for the first time, demonstrates TRIM16 is a marker of cell migration and metastasis, and a novel treatment target in melanoma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.