ReviewInternational journal of molecular sciences2019
Targeting Chemoresistant Tumors: Could TRIM Proteins-p53 Axis Be a Possible Answer?
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- TRIM27-Cas9-loaded EVs suppress HCC proliferation and enhance responsiveness to anti-PD-1 therapy by promoting ACSL4-mediated ferroptosis.Cell death and differentiation · 2026Article
- Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025Review
- Latest News from the "Guardian": p53 Directly Activates Asymmetric Stem Cell Division Regulators.International journal of molecular sciences · 2025Article
- Role of TRIM24 in the regulation of proteasome-autophagy crosstalk in bortezomib-resistant mantle cell lymphoma.Cell death discovery · 2025Article
- TRIM25: A Global Player of Cell Death Pathways and Promising Target of Tumor-Sensitizing Therapies.Cells · 2025Review
- TRIM25, TRIM28 and TRIM59 and Their Protein Partners in Cancer Signaling Crosstalk: Potential Novel Therapeutic Targets for Cancer.Current issues in molecular biology · 2024Review
- CircORC2 promoted proliferation and inhibited the sensitivity of osteosarcoma cell lines to cisplatin by regulating the miR-485-3p/TRIM2 axis.Journal of cell communication and signaling · 2024Article
- Article
- Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins.Cellular & molecular biology letters · 2024Review
- Comprehensive Analysis of the Prognostic Significance of the TRIM Family in the Context of TP53 Mutations in Cancers.Cancers · 2023Article
- circRNA_0067717 promotes paclitaxel resistance in nasopharyngeal carcinoma by acting as a scaffold for TRIM41 and p53.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- PDGFBB improved the biological function of menstrual blood-derived stromal cells and the anti-fibrotic properties of exosomes.Stem cell research & therapy · 2023Article
- Proteolytic regulation of CD73 by TRIM21 orchestrates tumor immunogenicity.Science advances · 2023Article
- Article
- TRIM21‑a potential biomarker for the prognosis of thyroid cancer.Experimental and therapeutic medicine · 2022Article
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- Stress-induced epinephrine promotes epithelial-to-mesenchymal transition and stemness of CRC through the CEBPB/TRIM2/P53 axis.Journal of translational medicine · 2022Article
- 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
- Identification of a tripartite motif family gene signature for predicting the prognosis of patients with glioma.American journal of translational research · 2022Article
- The roles and targeting options of TRIM family proteins in tumor.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemosensitivity is a crucial feature for all tumours so that they can be successfully treated, but the huge heterogeneity of these diseases, to be intended both inter- and intra-tumour, makes it a hard-to-win battle. Indeed, this genotypic and phenotypic variety, together with the adaptability of tumours, results in a plethora of chemoresistance acquisition mechanisms strongly affecting the effectiveness of treatments at different levels. Tripartite motif (TRIM) proteins are shown to be involved in some of these mechanisms thanks to their E3-ubiquitin ligase activity, but also to other activities they can exert in several cellular pathways. Undoubtedly, the ability to regulate the stability and activity of the p53 tumour suppressor protein, shared by many of the TRIMs, represents the preeminent link between this protein family and chemoresistance. Indeed, they can modulate p53 degradation, localization and subset of transactivated target genes, shifting the cellular response towards a cytoprotective or cytotoxic reaction to whatever damage induced by therapy, sometimes in a cellular-dependent way. The involvement in other chemoresistance acquisition mechanisms, independent by p53, is known, affecting pivotal processes like PI3K/Akt/NF-κB signalling transduction or Wnt/beta catenin pathway, to name a few. Hence, the inhibition or the enhancement of TRIM proteins functionality could be worth investigating to better understand chemoresistance and as a strategy to increase effectiveness of anticancer therapies.
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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 Socratic graph.