ReviewFrontiers in pharmacology2020
The Tripartite Nexus: Autophagy, Cancer, and Tripartite Motif-Containing Protein Family Members.
Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
- Infection and α-ketoglutarate/oxygen inhibition converge to CDC20 to promote cancer cell aneuploidy.Signal transduction and targeted therapy · 2026Article
- A role for CASM in the repair of damaged Golgi architecture.Autophagy · 2026Article
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- TRIM32 drives head and neck squamous cell carcinoma progression via TP53 suppression and lysosomal/autophagy dysregulation.Translational cancer research · 2026Article
- TRIM proteins as emerging regulators of immune pathways: potential therapeutic targets in immune-related disorders.Frontiers in immunology · 2026Review
- A role for CASM in the repair of damaged Golgi architecture.bioRxiv : the preprint server for biology · 2025Article
- TRIM21 functions as an oncogene in glioblastoma by transactivating FOSL1 and promoting the ubiquitination of p27.Cell communication and signaling : CCS · 2025Article
- The oncogenic role of TRIM56 in pancreatic cancer via the TRAF6/NF-kB axis.Journal of molecular histology · 2025Article
- Article
- The function of TRIML2 on the temozolomide resistance in glioblastoma.Annals of medicine and surgery (2012) · 2025Article
- TRIM25: A Global Player of Cell Death Pathways and Promising Target of Tumor-Sensitizing Therapies.Cells · 2025Review
- Construction and Validation of T-cell Exhaustion-related Gene Signature for Predicting Prognosis in Diffuse Large B-cell Lymphoma.Current pharmaceutical biotechnology · 2025Article
- TRIM-endous functional network of tripartite motif 29 (TRIM29) in cancer progression and beyond.Cancer metastasis reviews · 2024Review
- Trim13-induced ubiquitination of RPS27A inhibits the progression of lung cancer by depending on the inactivation of NF-κB signaling pathway.Physiological reports · 2024Article
- GDF11 inhibits the malignant progression of hepatocellular carcinoma via regulation of the mTORC1‑autophagy axis.Experimental and therapeutic medicine · 2024Article
- TRIM11 expression in non-small cell lung cancer is associated with poor prognosis.Histology and histopathology · 2024Article
- PRKAA2, MTOR, and TFEB in the regulation of lysosomal damage response and autophagy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- LncRNA OTUD6B-AS1 overexpression promoted GPX4-mediated ferroptosis to suppress radioresistance in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- The Functions of TRIM56 in Antiviral Innate Immunity and Tumorigenesis.International journal of molecular sciences · 2023Review
- TRIM8: a double-edged sword in glioblastoma with the power to heal or hurt.Cellular & molecular biology letters · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Autophagy is a cellular degradative process that has multiple important actions in cancer. Autophagy modulation is under consideration as a promising new approach to cancer therapy. However, complete autophagy dysregulation is likely to have substantial undesirable side effects. Thus, more targeted approaches to autophagy modulation may prove clinically beneficial. One potential avenue to achieving this goal is to focus on the actions of tripartite motif-containing protein family members (TRIMs). TRIMs have key roles in an array of cellular processes, and their dysregulation has been extensively linked to cancer risk and prognosis. As detailed here, emerging data shows that TRIMs can play important yet context-dependent roles in controlling autophagy and in the selective targeting of autophagic substrates. This review covers how the autophagy-related actions of TRIM proteins contribute to cancer and the possibility of targeting TRIM-directed autophagy in cancer therapy.
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What OpenQuestion holds
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.