ArticleMolecular cancer research : MCR2012
Inactivation of heat shock factor Hsf4 induces cellular senescence and suppresses tumorigenesis in vivo.
Article in Molecular cancer research : MCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
22 citing papers in PubMed, 29 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
- A guide to heat shock factors as multifunctional transcriptional regulators.The FEBS journal · 2025Review
- Potentiating doxorubicin activity through BCL-2 inhibition in p53 wild-type and mutated triple-negative breast cancer.Frontiers in oncology · 2025Article
- Association between heat shock factor protein 4 methylation and colorectal cancer risk and potential molecular mechanisms: A bioinformatics study.World journal of gastrointestinal oncology · 2023Article
- Stress-Inducible SCAND Factors Suppress the Stress Response and Are Biomarkers for Enhanced Prognosis in Cancers.International journal of molecular sciences · 2023Article
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
- FGD3 binds with HSF4 to suppress p65 expression and inhibit pancreatic cancer progression.Oncogene · 2022Article
- Stress Responses as Master Keys to Epigenomic Changes in Transcriptome and Metabolome for Cancer Etiology and Therapeutics.Molecular and cellular biology · 2022Article
- More Than Meets the Eye: Revisiting the Roles of Heat Shock Factor 4 in Health and Diseases.Biomolecules · 2021Review
- Identification of Transcription Factor-Related Gene Signature and Risk Score Model for Colon Adenocarcinoma.Frontiers in genetics · 2021Article
- Recurring Translocations in Barrett's Esophageal Adenocarcinoma.Frontiers in genetics · 2021Article
- Enhanced expression of queuine tRNA-ribosyltransferase 1 (Annals of translational medicine · 2020Article
- Review
- Transcriptome Differences Suggest Novel Mechanisms for Intrauterine Growth Restriction Mediated Dysfunction in Small Intestine of Neonatal Piglets.Frontiers in physiology · 2020Article
- The heat-shock, or HSF1-mediated proteotoxic stress, response in cancer: from proteomic stability to oncogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
- Transcription Factor and lncRNA Regulatory Networks Identify Key Elements in Lung Adenocarcinoma.Genes · 2018Article
- Targeted Deletion of Hsf1, 2, and 4 Genes in Mice.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Heat shock factor 2 is associated with the occurrence of lung cancer by enhancing the expression of heat shock proteins.Oncology letters · 2016Article
- Pleiotropic role of HSF1 in neoplastic transformation.Current cancer drug targets · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Studies suggest that Hsf4 expression correlates with its role in cell growth and differentiation. However, the role of Hsf4 in tumorigenesis in vivo remains unexplored. In this article, we provide evidence that absence of the Hsf4 gene suppresses evolution of spontaneous tumors arising in p53- or Arf-deficient mice. Furthermore, deletion of hsf4 alters the tumor spectrum by significantly inhibiting development of lymphomas that are normally observed in the majority of mice lacking p53 or Arf tumor suppressor genes. Using mouse embryo fibroblasts deficient in the hsf4 gene, we have found that these cells exhibit reduced proliferation that is associated with induction of senescence and senescence-associated β-galactosidase (SA-β-gal). Cellular senescence in hsf4-deficient cells is associated with the increased expression of the cyclin-dependent kinase inhibitors, p21 and p27 proteins. Consistent with the cellular senescence observed in vitro, specific normal tissues of hsf4(-/-) mice and tumors that arose in mice deficient in both hsf4 and p53 genes exhibit increased SA-β-gal activity and elevated levels of p27 compared with wild-type mice. These results suggest that hsf4 deletion-induced senescence is also present in vivo. Our results therefore indicate that Hsf4 is involved in modulation of cellular senescence, which can be exploited during cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.