Evidence map›Paper›PMID 31183804›Full record

ReviewCellular oncology (Dordrecht, Netherlands)2019

Interplay between HSF1 and p53 signaling pathways in cancer initiation and progression: non-oncogene and oncogene addiction.

Agnieszka Toma-Jonik, Natalia Vydra, Patryk Janus, Wiesława Widłak

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular oncology (Dordrecht, Netherlands), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. bioRxiv : the preprint server for biology · 2025
    Article
  4. Review
  5. Review
  6. Anchoring super-enhancer-driven oncogenic lncRNAs for anti-tumor therapy in hepatocellular carcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. The Emerging Role of Heat Shock Factor 1 (HSF1) and Heat Shock Proteins (HSPs) in Ferroptosis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Review
  11. HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023
    Review
  12. Review
  13. Article
  14. Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer's Disease?International journal of molecular sciences · 2022
    Review
  15. Article
  16. Proteasome regulators in pancreatic cancer.World journal of gastrointestinal oncology · 2022
    Review
  17. Review
  18. Article
  19. HighFrontiers in cell and developmental biology · 2021
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Agnieszka Toma-JonikMaria Skłodowska-Curie Institute - Oncology Center, Gliwice Branch, Wybrzeże Armii Krajowej 15, 44-101, Gliwice, Poland.
Natalia VydraMaria Skłodowska-Curie Institute - Oncology Center, Gliwice Branch, Wybrzeże Armii Krajowej 15, 44-101, Gliwice, Poland.
Patryk JanusMaria Skłodowska-Curie Institute - Oncology Center, Gliwice Branch, Wybrzeże Armii Krajowej 15, 44-101, Gliwice, Poland.
Wiesława WidłakMaria Skłodowska-Curie Institute - Oncology Center, Gliwice Branch, Wybrzeże Armii Krajowej 15, 44-101, Gliwice, Poland. wieslawa.widlak@io.gliwice.pl.ORCID http://orcid.org/0000-0002-8440-9414
The Maria Sklodowska-Curie National Research Institute of Oncology · PL

Funding

Narodowe Centrum Nauki 2014/13/B/NZ3/04650Narodowe Centrum Nauki 2014/13/B/NZ7/02341Narodowe Centrum Nauki 2015/17/B/NZ3/03760
6 · The paper itself

Abstract

backgroundThe p53 and HSF1 transcription factors are key players in cellular responses to stress. They activate important signaling pathways triggering adaptive mechanisms that maintain cellular homeostasis. HSF1 is mainly activated by proteotoxic stress, and its induction leads to the synthesis of chaperones that provide proteome integrity. The p53 protein, which is primarily activated in response to DNA damage, causes cell cycle arrest allowing for DNA repair or directs cells to apoptosis, thereby maintaining genome integrity. Both signaling pathways are also involved in neoplastic transformation and tumor progression. Loss of tumor suppressor abilities of the wild-type p53 protein results in oncogenesis, whereas proper HSF1 action, though non-oncogenic itself, actively supports this process.

conclusionsHere, we describe in detail the interplay between the p53 and HSF1 signaling pathways, with particular emphasis on the molecular mechanisms involved, as well as their importance for normal cellular behavior, cancer development, the effectiveness of anti-cancer therapies and their toxicity. Detailed knowledge of the complex interplay between HSF1 and p53 may form a basis for the design of new protocols for cancer treatment.

Indexed as

AnimalsApoptosisCarcinogenesisCellular SenescenceCytoprotectionDisease ProgressionDNA RepairHost Cell Factor C1HumansImmediate-Early ProteinsNeovascularization, PathologicNuclear ProteinsOncogene AddictionSignal TransductionStress, PhysiologicalTumor Suppressor Protein p53HCFC1 protein, humanHost Cell Factor C1IER5 protein, humanImmediate-Early ProteinsNuclear ProteinsTumor Suppressor Protein p53HSF1Oncogenesisp53Transcription factors

Identifiers

PMID31183804
PMCPMC12994296
OpenAlexW2953260398

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.