ReviewGenes2018
TRAP1 Regulation of Cancer Metabolism: Dual Role as Oncogene or Tumor Suppressor.
Review in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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.
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Who cites it
58 citing papers in PubMed, 103 citations in OpenAlex.
- Exploring the lactate-metabolism related characteristics during the development of medulloblastoma through single-cell and bulk RNA-seq.Translational cancer research · 2026Article
- Establishment of a mInternational journal of genomics · 2026Article
- Comprehensive pan-cancer analysis of TRAP1 and its experimental validation in hepatocellular carcinoma.Discover oncology · 2025Article
- Cancer suppresses mitochondrial chaperone activity in macrophages to drive immune evasion.Nature immunology · 2025Article
- The molecular chaperone TRAP1 promotes translation ofRNA (New York, N.Y.) · 2025Article
- Mitochondrial HSP90 Paralog TRAP1 Deletion Drives Glutamine Addiction in Tumor Cells via Destablization of the Cys/Glu Antiporter SLC7A11/xCT.Molecular cancer research : MCR · 2025Article
- The examination of in vitro photosensitizing efficacy of aloe-emodin loaded liposome following photodynamic therapy on melanoma cell lines.Scientific reports · 2025Article
- Tumor necrosis factor receptor-associated protein 1 promotes aerobic glycolysis and cisplatin resistance by regulating the Wnt/β-catenin signaling pathway in lung cancer.Histology and histopathology · 2025Article
- Immune evasion in cancer: mechanisms and cutting-edge therapeutic approaches.Signal transduction and targeted therapy · 2025Review
- Ochratoxin A-induced mitochondrial pathway apoptosis and ferroptosis by promoting glycolysis.Apoptosis : an international journal on programmed cell death · 2025Article
- Targeting HSP90 in Gynecologic Cancer: Molecular Mechanisms and Therapeutic Approaches.Cell biochemistry and biophysics · 2025Review
- TRAP1 Improves Diabetic Retinopathy by Preserving Mitochondrial Function.Clinical ophthalmology (Auckland, N.Z.) · 2025Article
- TRAP1 induced cisplatin resistance in gastric cancer cells by regulating oxidative stress.Frontiers in molecular biosciences · 2025Article
- TRAP1 functions in the morphogenesis of the embryonic kidney.Animal cells and systems · 2025Article
- Comprehensive overview of how to fade into succinate dehydrogenase dysregulation in cancer cells by naringenin-loaded chitosan nanoparticles.Genes & nutrition · 2024Review
- Myriad factors and pathways influencing tumor radiotherapy resistance.Open life sciences · 2024Review
- Ecological network analysis reveals cancer-dependent chaperone-client interaction structure and robustness.Nature communications · 2023Article
- Inhibition of TRAP1 Accelerates the DNA Damage Response, Activation of the Heat Shock Response and Metabolic Reprogramming in Colon Cancer Cells.Frontiers in bioscience (Landmark edition) · 2023Article
- Cytosolic and mitochondrial translation elongation are coordinated through the molecular chaperone TRAP1 for the synthesis and import of mitochondrial proteins.Genome research · 2023Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming is an important issue in tumor biology. An unexpected inter- and intra-tumor metabolic heterogeneity has been strictly correlated to tumor outcome. Tumor Necrosis Factor Receptor-Associated Protein 1 (TRAP1) is a molecular chaperone involved in the regulation of energetic metabolism in cancer cells. This protein is highly expressed in several cancers, such as glioblastoma, colon, breast, prostate and lung cancers and is often associated with drug resistance. However, TRAP1 is also downregulated in specific tumors, such as ovarian, bladder and renal cancers, where its lower expression is correlated with the worst prognoses and chemoresistance. TRAP1 is the only mitochondrial member of the Heat Shock Protein 90 (HSP90) family that directly interacts with respiratory complexes, contributing to their stability and activity but it is still unclear if such interactions lead to reduced or increased respiratory capacity. The role of TRAP1 is to enhance or suppress oxidative phosphorylation; the effects of such regulation on tumor development and progression are controversial. These observations encourage the study of the mechanisms responsible for the dualist role of TRAP1 as an oncogene or oncosuppressor in specific tumor types. In this review, TRAP1 puzzling functions were recapitulated with a special focus on the correlation between metabolic reprogramming and tumor outcome. We wanted to investigate whether metabolism-targeting drugs can efficiently interfere with tumor progression and whether they might be combined with chemotherapeutics or molecular-targeted agents to counteract drug resistance and reduce therapeutic failure.
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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.