ArticleOncogene2016
Heat-shock factor 2 is a suppressor of prostate cancer invasion.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
- 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
- Heat shock transcription factors in development and disease.Disease models & mechanisms · 2026Review
- HSF2 drives breast cancer progression by acting as a stage-specific switch between proliferation and invasion.Science advances · 2025Article
- A guide to heat shock factors as multifunctional transcriptional regulators.The FEBS journal · 2025Review
- Exploring the impact of cuproptosis on prostate cancer prognosisFrontiers in pharmacology · 2025Article
- Review
- Heat shock transcription factor 1 facilitates liver cancer progression by driving super-enhancer-mediated transcription of MYCN.Cancer medicine · 2024Article
- Targeting the cancer cells and cancer-associated fibroblasts with next-generation FGFR inhibitors in prostate cancer co-culture models.Cancer medicine · 2024Article
- Linking Gene Fusions to Bone Marrow Failure and Malignant Transformation in Dyskeratosis Congenita.International journal of molecular sciences · 2024Article
- Cancer cell invasion alters the protein profile of extracellular vesicles.Journal of extracellular biology · 2023Article
- HSF4 promotes tumor progression of colorectal cancer by transactivating c-MET.Molecular and cellular biochemistry · 2023Article
- Heat Shock Transcription Factor 2 Is Significantly Involved in Neurodegenerative Diseases, Inflammatory Bowel Disease, Cancer, Male Infertility, and Fetal Alcohol Spectrum Disorder: The Novel Mechanisms of Several Severe Diseases.International journal of molecular sciences · 2022Review
- Aberrant HSF1 signaling activation underlies metformin amelioration of myocardial infarction in mice.Molecular therapy. Nucleic acids · 2022Article
- HSF2 cooperates with HSF1 to drive a transcriptional program critical for the malignant state.Science advances · 2022Article
- 3D Cell Cultures: Evolution of an Ancient Tool for New Applications.Frontiers in physiology · 2022Review
- Heat Shock Proteins and HSF1 in Cancer.Frontiers in oncology · 2022Review
- The heat shock response and small molecule regulators.European journal of medicinal chemistry · 2021Review
- Gambogic acid and gambogenic acid induce a thiol-dependent heat shock response and disrupt the interaction between HSP90 and HSF1 or HSF2.Cell stress & chaperones · 2021Article
- Gene networks and transcriptional regulators associated with liver cancer development and progression.BMC medical genomics · 2021Article
- The proteostasis guardian HSF1 directs the transcription of its paralog and interactor HSF2 during proteasome dysfunction.Cellular and molecular life sciences : CMLS · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat-shock factors (HSFs) are key transcriptional regulators in cell survival. Although HSF1 has been identified as a driver of carcinogenesis, HSF2 has not been explored in malignancies. Here, we report that HSF2 suppresses tumor invasion of prostate cancer (PrCa). In three-dimensional organotypic cultures and the in vivo xenograft chorioallantoic membrane model HSF2 knockdown perturbs organoid differentiation and promotes invasiveness. Gene expression profiling together with functional studies demonstrated that the molecular mechanism underlying the effect on tumor progression originates from HSF2 steering the switch between acinar morphogenesis and invasion. This is achieved by the regulation of genes connected to, for example, GTPase activity, cell adhesion, extracellular matrix and actin cytoskeleton dynamics. Importantly, low HSF2 expression correlates with high Gleason score, metastasis and poor survival of PrCa patients, highlighting the clinical relevance of our findings. Finally, the study was expanded beyond PrCa, revealing that the expression of HSF2 is decreased in a wide range of cancer types. This study provides the first evidence for HSF2 acting as a suppressor of invasion in human malignancies.
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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.