Evidence map›Paper›PMID 29728578›Full record

ArticleScientific reports2018

Propranolol sensitizes prostate cancer cells to glucose metabolism inhibition and prevents cancer progression.

Laura Brohée, Olivier Peulen, Betty Nusgens, Vincent Castronovo, Marc Thiry, Alain C Colige, Christophe F Deroanne

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 76 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Drug repurposing in oncology: a path beyond the bottleneck.Medical oncology (Northwood, London, England) · 2025
    Review
  7. Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. The multifaceted role of beta-blockers in overcoming cancer progression and drug resistance: Extending beyond cardiovascular disorders.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Targeting the βThe Journal of pathology · 2023
    Article
  19. 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

7 authors at 1 institution in 1 country.

Laura BrohéeLaboratory of Connective Tissues Biology, GIGA-Cancer, University of Liège, 4000, Liège, Belgium.
Olivier PeulenMetastasis Research Laboratory, GIGA-Cancer, University of Liège, 4000, Liège, Belgium.ORCID 0000-0002-6933-0134
Betty NusgensLaboratory of Connective Tissues Biology, GIGA-Cancer, University of Liège, 4000, Liège, Belgium.
Vincent CastronovoMetastasis Research Laboratory, GIGA-Cancer, University of Liège, 4000, Liège, Belgium.
Marc ThiryLaboratory of Cell Biology, GIGA-R, University of Liège, 20 rue des Pitteurs, 4020, Liège, Belgium.
Alain C ColigeLaboratory of Connective Tissues Biology, GIGA-Cancer, University of Liège, 4000, Liège, Belgium.
Christophe F DeroanneLaboratory of Connective Tissues Biology, GIGA-Cancer, University of Liège, 4000, Liège, Belgium. c.deroanne@uliege.be.
University of Liège · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Propranolol, a widely used non-selective beta-adrenergic receptor blocker, was recently shown to display anticancer properties. Its potential to synergize with certain drugs has been also outlined. However, it is necessary to take into account all the properties of propranolol to select a drug that could be efficiently combined with. Propranolol was reported to block the late phase of autophagy. Hence, we hypothesized that in condition enhancing autophagy flux, cancer cells should be especially sensitive to propranolol. 2DG, a glycolysis inhibitor, is an anti-tumor agent having limited effect in monotherapy notably due to induction of pro-survival autophagy. Here, we report that treatment of cancer cells with propranolol in combination with the glycolysis inhibitor 2DG induced a massive accumulation of autophagosome due to autophagy blockade. The propranolol +2DG treatment efficiently prevents prostate cancer cell proliferation, induces cell apoptosis, alters mitochondrial morphology, inhibits mitochondrial bioenergetics and aggravates ER stress in vitro and also suppresses tumor growth in vivo. Our study underlines for the first time the interest to take advantage of the ability of propranolol to inhibit autophagy to design new anti-cancer therapies.

Indexed as

AnimalsAutophagyCarbohydrate MetabolismCell Line, TumorDisease Models, AnimalDisease ProgressionEndoplasmic Reticulum StressGlucoseGlycolysisHumansMaleMiceMitochondriaPropranololProstatic NeoplasmsXenograft Model Antitumor AssaysGlucosePropranolol

Identifiers

PMID29728578
PMCPMC5935740
OpenAlexW2807188419

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.