ArticleCancer research2024
HSF1 Inhibits Antitumor Immune Activity in Breast Cancer by Suppressing CCL5 to Block CD8+ T-cell Recruitment.
Article in Cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- Tumor-intrinsic NSUN2 orchestrates immunosuppression in lung adenocarcinoma via the mExperimental hematology & oncology · 2026Article
- Immune Circuit Rewiring by HDAC Inhibition Enables Response to Dual Checkpoint Blockade in Metastatic Breast Cancer.Cancer research · 2026Article
- Unveiling CCL5: the master regulator of breast cancer progression and immune evasion.Breast cancer research : BCR · 2026Review
- Single-cell profiling reveals peripheral blood immune landscape remodelling in breast cancer lymph node metastasis.Clinical and translational medicine · 2026Article
- Heat shock transcription factors in development and disease.Disease models & mechanisms · 2026Review
- Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin.Journal of experimental & clinical cancer research : CR · 2025Article
- CCL5Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Dynamic remodelling of epithelial plasticity in colorectal cancer from single-cell and spatially resolved perspectives.Journal of translational medicine · 2025Article
- Targeting SHP2 to reverse immune evasion and resistance to anti-PD-1 therapy in non-small cell lung cancer.Cell communication and signaling : CCS · 2025Article
- Single-cell transcriptomics of the myeloid milieu reveals an angiogenic niche in triple-negative breast cancer.Experimental & molecular medicine · 2025Article
- Identification of a novel m6A RNA methylation regulator-based signature for prognosis and immune landscape prediction in hepatocellular carcinoma.Scientific reports · 2025Article
- HSF1-DBC1 axis drives prostate cancer progression by activating a metastatic transcriptional program.Experimental & molecular medicine · 2025Article
- HSF2 drives breast cancer progression by acting as a stage-specific switch between proliferation and invasion.Science advances · 2025Article
- A multifunctional biomimetic nanoplatform combined with immune checkpoint blockade for triple-negative breast cancer immunotherapy through inhibiting polarization of M2 macrophages.Journal of nanobiotechnology · 2025Article
- A guide to heat shock factors as multifunctional transcriptional regulators.The FEBS journal · 2025Review
- Chemical engineering of γδ T cells with cancer cell-targeting antibodies for enhanced tumor immunotherapy.National science review · 2025Article
- Deciphering of intra-tumoural heterogeneity and the interplay between metastasis-associated meta-program and myofibroblasts in gastric cancer.Clinical and translational medicine · 2025Article
- Role of HSF1 in cell division, tumorigenesis and therapy: a literature review.Cell division · 2025Review
- [Public Database-based Study to Explore the Expression and Role of DDB1 in Lung Adenocarcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Heat shock factor 1 (HSF1) is a stress-responsive transcription factor that promotes cancer cell malignancy. To provide a better understanding of the biological processes regulated by HSF1, here we developed an HSF1 activity signature (HAS) and found that it was negatively associated with antitumor immune cells in breast tumors. Knockdown of HSF1 decreased breast tumor size and caused an influx of several antitumor immune cells, most notably CD8+ T cells. Depletion of CD8+ T cells rescued the reduction in growth of HSF1-deficient tumors, suggesting HSF1 prevents CD8+ T-cell influx to avoid immune-mediated tumor killing. HSF1 suppressed expression of CCL5, a chemokine for CD8+ T cells, and upregulation of CCL5 upon HSF1 loss significantly contributed to the recruitment of CD8+ T cells. These findings indicate that HSF1 suppresses antitumor immune activity by reducing CCL5 to limit CD8+ T-cell homing to breast tumors and prevent immune-mediated destruction, which has implications for the lack of success of immune modulatory therapies in breast cancer. SIGNIFICANCE: The stress-responsive transcription factor HSF1 reduces CD8+ T-cell infiltration in breast tumors to prevent immune-mediated killing, indicating that cellular stress responses affect tumor-immune interactions and that targeting HSF1 could improve immunotherapies.
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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.