ArticleCell death & disease2025
Heat shock factor 1 promotes proliferation and chemoresistance in diffuse large B-cell lymphoma by enhancing the cell cycle and DNA repair.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Adaptation to heat stress by diversification of the vertebrate heat shock transcription factor family.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- DIXDC1 Promotes Lymphatic Metastasis and Resistance to Cuproptosis in Bladder Cancer Through Mediating DLAT.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- METTL3-dependent mJournal of translational medicine · 2026Article
- In Silico Perturbation Identifies Transcription Factors as Protective Targets in HSPCs After Irradiation.International journal of molecular sciences · 2026Article
- The Art of Domesticating Proteins: How Cancer Cells Adapt to Therapeutic and Environmental Stressors.International journal of molecular sciences · 2026Review
- Inhibition of autoantigen-induced B-cell receptor (BCR) internalization as a therapeutic strategy in diffuse large B cell lymphoma (DLBCL).Cell death & disease · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Diffuse large B-cell lymphoma (DLBCL) is commonly treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), but up to 40% of patients have refractory or relapsing disease and show unsatisfactory responses to salvage treatment. Heat shock factor 1 (HSF1) regulates the transcription of a group of oncogenes, promoting chemoresistance and representing a promising therapeutic target. However, the role and mechanism of HSF1 in DLBCL remain unknown. In this study, we discovered that the overexpression of HSF1 was correlated with unfavorable treatment response and poor prognosis in patients with DLBCL. Inhibition of HSF1 via shRNA or DTHIB, a pharmacological inhibitor of HSF1, inhibited cell proliferation and increased chemosensitivity to vincristine and doxorubicin both in vitro and in vivo. Mechanistically, we revealed that genes related to the cell cycle, DNA repair, and p53 signalling pathways, including CCNB1, CCNE2, E2F2, and XRCC2, were directly regulated by HSF1 in a protein arginine methyltransferase 5 (PRMT5) -dependent manner. These findings demonstrated that the significant transcriptional regulator HSF1 promoted cell proliferation and chemoresistance in DLBCL. Targeting HSF1 may serve as a promising therapeutic strategy that enhances the antitumor effects of chemotherapy in DLBCL.
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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.