ArticleOncology reports2017
TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway.
Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03467308 (Identification of New Signaling Pathways Targeting Colorectal Cancer in Egyptian Patients), which is not on this map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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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
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.
Identification of New Signaling Pathways Targeting Colorectal Cancer in Egyptian Patients
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Prognostic significance of TRIM59 for cancer patient survival: A systematic review and meta-analysis.Medicine · 2019Pooled it
- TRIM25, TRIM28 and TRIM59 and Their Protein Partners in Cancer Signaling Crosstalk: Potential Novel Therapeutic Targets for Cancer.Current issues in molecular biology · 2024Review
- E3 ubiquitin ligase BTBD3 inhibits tumorigenesis of colorectal cancer by regulating the TYRO3/Wnt/β-catenin signaling axis.Cancer cell international · 2024Article
- TRIM59 deficiency promotes M1 macrophage activation and inhibits colorectal cancer through the STAT1 signaling pathway.Scientific reports · 2024Article
- IGF2BP2-m6A-circMMP9 axis recruits ETS1 to promote TRIM59 transcription in laryngeal squamous cell carcinoma.Scientific reports · 2024Article
- Exploring the Mechanisms, Biomarkers, and Therapeutic Targets of TRIM Family in Gastrointestinal Cancer.Drug design, development and therapy · 2024Review
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- TargetingGastroenterology report · 2023Review
- TRIM59 guards ER proteostasis and prevents Bortezomib-mediated colorectal cancer (CRC) cells' killing.Investigational new drugs · 2022Article
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- The roles and targeting options of TRIM family proteins in tumor.Frontiers in pharmacology · 2022Review
- Article
- Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging.Genome biology · 2021Article
- Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells-Relevance for Understanding (Germ Cell) Tumorigenesis.International journal of molecular sciences · 2021Review
- TRIM39 deficiency inhibits tumor progression and autophagic flux in colorectal cancer via suppressing the activity of Rab7.Cell death & disease · 2021Article
- TRIM Proteins in Colorectal Cancer: TRIM8 as a Promising Therapeutic Target in Chemo Resistance.Biomedicines · 2021Review
- Regulation of p53 by E3s.Cancers · 2021Review
- Article
- Prognostic Factors of Colorectal Cancer: A Comparative Study on Patients With or Without Liver Metastasis.Frontiers in oncology · 2021Article
- Multifaceted Roles of TRIM Proteins in Colorectal Carcinoma.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif-containing 59 (TRIM59) belongs to the tripartite motif (TRIM) protein family and is upregulated in various malignancies. However, its expression in colorectal cancer (CRC) is still unknown. In the present study, we examined the expression and biological function of TRIM59 in CRC. We analyzed CRC tissues and cells by quantitative real-time polymerase chain reaction. Kaplan-Meier survival analysis was used to evaluate the prognostic significance of TRIM59 in CRC patients. Furthermore, we investigated the role of TRIM59 in CRC growth and metastasis. The potential mechanism underlying the regulation of cell metastasis by TRIM59 was determined by western blotting. TRIM59 expression was conspicuously overexpressed in CRC tissues and CRC cell lines compared to that noted in the corresponding normal control cells. Patients with higher TRIM59 expression had poorer prognosis. Furthermore, knockdown of TRIM59 suppressed cell proliferation through the induction of apoptosis and inhibited migration and invasion significantly in vitro. Further investigation revealed that knockdown of TRIM59 effectively reversed the expression of epithelial-mesenchymal transformation‑related proteins vimentin, Snail and E-cadherin. Our preliminary results confirm that TRIM59 can be mediated by PI3K/AKT signaling. TRIM59 functions as an oncogene in CRC progression, which could be a novel target for the detection and treatment of CRC.
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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.