Evidence map›Paper›PMID 27416726›Full record

ArticleBMC cancer2016

Bile acids destabilise HIF-1α and promote anti-tumour phenotypes in cancer cell models.

J P Phelan, F J Reen, N Dunphy, R O'Connor, F O'Gara

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Hypoxia-inducible factor-driven glycolytic adaptations in host-microbe interactions.Pflugers Archiv : European journal of physiology · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Efflux, Signaling and Warfare in a Polymicrobial World.Antibiotics (Basel, Switzerland) · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Plasma Metabolic Phenotypes of HPV-Associated versus Smoking-Associated Head and Neck Cancer and Patient Survival.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
    Article
  14. Review
  15. Research Progress of Bile Acids in Cancer.Frontiers in oncology · 2021
    Review
  16. Review
  17. Review
  18. Review
  19. Liver- and Microbiome-derived Bile Acids Accumulate in Human Breast Tumors and Inhibit Growth and Improve Patient Survival.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  20. Review
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

5 authors at 2 institutions in 2 countries.

J P PhelanBIOMERIT Research Centre, School of Microbiology, University College Cork - National University of Ireland, Cork, Ireland.
F J ReenBIOMERIT Research Centre, School of Microbiology, University College Cork - National University of Ireland, Cork, Ireland.
N DunphyBIOMERIT Research Centre, School of Microbiology, University College Cork - National University of Ireland, Cork, Ireland.
R O'ConnorSchool of Biochemistry and Cell Biology, University College Cork - National University of Ireland, Cork, Ireland.
F O'GaraBIOMERIT Research Centre, School of Microbiology, University College Cork - National University of Ireland, Cork, Ireland. f.ogara@ucc.ie.
University College Cork · IENational University of Ireland · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of the microbiome has become synonymous with human health and disease. Bile acids, as essential components of the microbiome, have gained sustained credibility as potential modulators of cancer progression in several disease models. At physiological concentrations, bile acids appear to influence cancer phenotypes, although conflicting data surrounds their precise physiological mechanism of action. Previously, we demonstrated bile acids destabilised the HIF-1α subunit of the Hypoxic-Inducible Factor-1 (HIF-1) transcription factor. HIF-1 overexpression is an early biomarker of tumour metastasis and is associated with tumour resistance to conventional therapies, and poor prognosis in a range of different cancers.

methodsHere we investigated the effects of bile acids on the cancer growth and migratory potential of cell lines where HIF-1α is known to be active under hypoxic conditions. HIF-1α status was investigated in A-549 lung, DU-145 prostate and MCF-7 breast cancer cell lines exposed to bile acids (CDCA and DCA). Cell adhesion, invasion, migration was assessed in DU-145 cells while clonogenic growth was assessed in all cell lines.

resultsIntracellular HIF-1α was destabilised in the presence of bile acids in all cell lines tested. Bile acids were not cytotoxic but exhibited greatly reduced clonogenic potential in two out of three cell lines. In the migratory prostate cancer cell line DU-145, bile acids impaired cell adhesion, migration and invasion. CDCA and DCA destabilised HIF-1α in all cells and significantly suppressed key cancer progression associated phenotypes; clonogenic growth, invasion and migration in DU-145 cells.

conclusionsThese findings suggest previously unobserved roles for bile acids as physiologically relevant molecules targeting hypoxic tumour progression.

Indexed as

ApoptosisBile Acids and SaltsCell AdhesionCell Line, TumorCell MovementCell ProliferationHumansHypoxia-Inducible Factor 1, alpha SubunitPhenotypeProtein StabilityBile Acids and SaltsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitBile acidsCancer modelsDimethyloxaloglycine (DMOG)HIF-1 transcription factorHIF-1α subunitHypoxia

Identifiers

PMID27416726
PMCPMC4946243
OpenAlexW2467519122

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.