ReviewFrontiers in oncology2022
Heat Shock Proteins and HSF1 in Cancer.
Review in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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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
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Machine learning-based analysis of cancer cell-derived vesicular proteins revealed significant tumor-specificity and predictive potential of extracellular vesicles for cell invasion and proliferation - A meta-analysis.Cell communication and signaling : CCS · 2023Pooled it
- Review
- Development of a multi-targeted sulfonyl-bridged bisselenadiazole derivative as a potent EGFR/PI3K/AKT/mTOR modulator in lung adenocarcinoma.RSC advances · 2026Article
- The Novel HSF1 Inhibitor NXP800 Exhibits Robust Antitumor Activity in Hepatocellular Carcinoma.International journal of molecular sciences · 2026Article
- Prolonged Oxidative Stress Drives p53/p21-Mediated Senescence and Degenerative Adaptation in Kidney-Derived Cells.Oxidative medicine and cellular longevity · 2026Article
- Polyploid giant cancer cells (PGCC): short-term return to multicellularity.Biological research · 2025Article
- A default silencing mechanism restrains stress-induced genes inbioRxiv : the preprint server for biology · 2025Article
- Article
- Navigating the landscape of protein folding and proteostasis: from molecular chaperones to therapeutic innovations.Signal transduction and targeted therapy · 2025Review
- HSF1-DBC1 axis drives prostate cancer progression by activating a metastatic transcriptional program.Experimental & molecular medicine · 2025Article
- HSP90 and the cancer transcriptome: a comprehensive review of inhibitors and mechanistic insights.International journal of clinical oncology · 2025Review
- Human milk-derived extracellular vesicles promote the heat shock response in polarized microglia.Cell stress & chaperones · 2025Article
- Identifying Cellular Stress-Related mRNA Changes Induced by Novel Xanthone Derivatives in Ovarian Cancer Cells In Vitro.Pharmaceutics · 2025Article
- Nuclear SUMOylation and Proteotoxic Stress Responses to Metals with Different Ligand Preferences.Chemical research in toxicology · 2025Article
- Identifying Genes Associated with the Anticancer Activity of a Fluorinated Chalcone in Triple-Negative Breast Cancer Cells Using Bioinformatics Tools.International journal of molecular sciences · 2025Article
- Knockdown of HSF1 inhibits invasion, metastasis, and proliferation of endometrial carcinoma cells while promoting apoptosis.Cancer biomarkers : section A of Disease markers · 2025Article
- Targeting HSP90 in Gynecologic Cancer: Molecular Mechanisms and Therapeutic Approaches.Cell biochemistry and biophysics · 2025Review
- Article
- Transcriptomics Unveil Canonical and Non-Canonical Heat Shock-Induced Pathways in Human Cell Lines.International journal of molecular sciences · 2025Article
- Synergistic effects of 6-shogaol and hyperthermia on ACHN renal cancer cells: modulation of ROS and heat shock pro-teins in cancer therapy.Frontiers in pharmacology · 2025Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fitness of cells is dependent on protein homeostasis which is maintained by cooperative activities of protein chaperones and proteolytic machinery. Upon encountering protein-damaging conditions, cells activate the heat-shock response (HSR) which involves HSF1-mediated transcriptional upregulation of a group of chaperones - the heat shock proteins (HSPs). Cancer cells experience high levels of proteotoxic stress due to the production of mutated proteins, aneuploidy-induced excess of components of multiprotein complexes, increased translation rates, and dysregulated metabolism. To cope with this chronic state of proteotoxic stress, cancers almost invariably upregulate major components of HSR, including HSF1 and individual HSPs. Some oncogenic programs show dependence or coupling with a particular HSR factor (such as frequent coamplification of HSF1 and MYC genes). Elevated levels of HSPs and HSF1 are typically associated with drug resistance and poor clinical outcomes in various malignancies. The non-oncogene dependence ("addiction") on protein quality controls represents a pancancer target in treating human malignancies, offering a potential to enhance efficacy of standard and targeted chemotherapy and immune checkpoint inhibitors. In cancers with specific dependencies, HSR components can serve as alternative targets to poorly druggable oncogenic drivers.
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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.