ArticleMolecular therapy : the journal of the American Society of Gene Therapy2018
Heat Shock Factor 1 Epigenetically Stimulates Glutaminase-1-Dependent mTOR Activation to Promote Colorectal Carcinogenesis.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 94 citations in OpenAlex.
- Multi-omics and bulk sequencing analyses reveal the roles of prognosis and immune aspects of super-enhancer-induced ZBED2 in pan-cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Glutaminase 1 in Vascular Disease: Linking Metabolic Reprogramming to Atherosclerosis Progression and Stability.Journal of cardiovascular translational research · 2026Review
- Human DEAH-box helicase 8 regulates HSF1-mediated stress response and cancer-associated pre-mRNA splicing in tumour cells.NAR cancer · 2026Article
- Identification of super-enhancer-based biomarkers for predicting survival and immunotherapy efficacy in colorectal cancer.Journal of Cancer · 2026Article
- Prognostic signature and tumor microenvironment infiltration based on amino acid metabolism-related genes and lncRNAs of colorectal cancer.Scientific reports · 2025Article
- Crosstalk Between Metabolic Reprogramming and Epigenetic Modifications in Colorectal Cancer: Mechanisms and Clinical Applications.Current issues in molecular biology · 2025Review
- Enhancement of colorectal cancer therapy through interruption of the HSF1-HSP90 axis by p53 activation or cell cycle inhibition.Cell death and differentiation · 2025Article
- The impact of stress in domestic animals: roles of heat shock proteins and acute-phase proteins.Veterinary research communications · 2025Review
- Colorectal Cancer: Pathogenesis and Targeted Therapy.MedComm · 2025Review
- Metabolic Targets in CRC: The Emerging Role of Cytochrome P450 Inhibitors.Current pharmaceutical design · 2025Review
- Review
- An HSF1-JMJD6-HSP feedback circuit promotes cell adaptation to proteotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Glutaminolysis regulates endometrial fibrosis in intrauterine adhesion via modulating mitochondrial function.Biological research · 2024Article
- Glutamine suppresses senescence and promotes autophagy through glycolysis inhibition-mediated AMPKα lactylation in intervertebral disc degeneration.Communications biology · 2024Article
- The roles and molecular mechanisms of non-coding RNA in cancer metabolic reprogramming.Cancer cell international · 2024Review
- Article
- Heat Shock Proteins and Breast Cancer.International journal of molecular sciences · 2024Review
- PRMT6-mediated ADMA promotes p62 phase separation to form a negative feedback loop in ferroptosis.Theranostics · 2024Article
- Proteomic characterization of the colorectal cancer response to chemoradiation and targeted therapies reveals potential therapeutic strategies.Cell reports. Medicine · 2023Article
- Inflammatory Bowel Diseases: An Updated Overview on the Heat Shock Protein Involvement.International journal of molecular sciences · 2023Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat shock factor 1 (HSF1) generally exhibits its properties under stress conditions. In tumors, HSF1 has a pleiotropic feature in regulating growth, survival, and aggressiveness of cancer cells. In this study, we found HSF1 was increased in colorectal cancer (CRC) and had a positive correlation with shorter disease-free survival (DFS). Knockdown of HSF1 in CRC cells attenuated their growth while inhibiting mTOR activation and glutamine metabolism. HSF1 inhibited the expression of microRNA137 (MIR137), which targeted GLS1 (glutaminase 1), thus stimulating GLS1 protein expression to promote glutaminolysis and mTOR activation. HSF1 bound DNA methyltransferase DNMT3a and recruited it to the promoter of lncRNA MIR137 host gene (MIR137HG), suppressing the generation of primary MIR137. The chemical inhibitor of HSF1 also reduced cell growth, increased apoptosis, and impaired glutamine metabolism in vitro. Moreover, both chemical inhibition and genetic knockout of HSF1 succeeded in increasing MIR137 expression, reducing GLS1 expression, and alleviating colorectal tumorigenesis in azoxymethane (AOM)/dextran sulfate sodium (DSS) mice. In conclusion, HSF1 expression was increased and associated with poor prognosis in CRC. By recruiting DNMT3a to suppress the expression of MIR137 that targets GLS1 mRNA, HSF1 stimulated GLS1-dependent mTOR activation to promote colorectal carcinogenesis. Therefore, targeting HSF1 to attenuate glutaminolysis and mTOR activation could be a promising approach for CRC treatment.
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