Evidence map›Paper›PMID 23764845›Full record

ArticleCell death & disease2013

Cannabinoids inhibit energetic metabolism and induce AMPK-dependent autophagy in pancreatic cancer cells.

I Dando, M Donadelli, C Costanzo, E Dalla Pozza, A D'Alessandro, L Zolla, M Palmieri

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 5 pooled it
6.0field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 5 syntheses or guidelines pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. Scoping Review and Meta-Analysis Suggests thatCannabis and cannabinoid research · 2021
    Pooled it
  3. Guideline
  4. Glucose metabolic phenotype of pancreatic cancer.World journal of gastroenterology · 2016
    Pooled it
  5. Guideline
  6. Trial
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. The role of AMPK in pancreatic cancer: from carcinogenesis to treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  17. Review
  18. Article
  19. Review
  20. Inflammation and cancer: friend or foe?Frontiers in pharmacology · 2024
    Review

20 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

I DandoDepartment of Life and Reproduction Sciences, Biochemistry Section, University of Verona, Verona, Italy.
M Donadelli
C Costanzo
E Dalla Pozza
A D'Alessandro
L Zolla
M Palmieri
University of Verona · ITUniversità degli Studi della Tuscia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The anti-tumoral effects of cannabinoids have been described in different tumor systems, including pancreatic adenocarcinoma, but their mechanism of action remains unclear. We used cannabinoids specific for the CB1 (ACPA) and CB2 (GW) receptors and metabolomic analyses to unravel the potential pathways mediating cannabinoid-dependent inhibition of pancreatic cancer cell growth. Panc1 cells treated with cannabinoids show elevated AMPK activation induced by a ROS-dependent increase of AMP/ATP ratio. ROS promote nuclear translocation of GAPDH, which is further amplified by AMPK, thereby attenuating glycolysis. Furthermore, ROS determine the accumulation of NADH, suggestive of a blockage in the respiratory chain, which in turn inhibits the Krebs cycle. Concomitantly, inhibition of Akt/c-Myc pathway leads to decreased activity of both the pyruvate kinase isoform M2 (PKM2), further downregulating glycolysis, and glutamine uptake. Altogether, these alterations of pancreatic cancer cell metabolism mediated by cannabinoids result in a strong induction of autophagy and in the inhibition of cell growth.

Indexed as

AutophagyAcetylcysteineAdenocarcinomaAdenosine MonophosphateAdenosine TriphosphateAdenylate KinaseAntineoplastic AgentsArachidonic AcidsCannabinoidsCell Line, TumorCell NucleusCitric Acid CycleDrug Screening Assays, AntitumorEnergy MetabolismEnzyme ActivationGlutamine1-(2,3-dichlorobenzoyl)-5-methoxy-2-methyl-(2-(mopholin-4-yl)ethyl)-1H-indoleAcetylcysteineAdenosine MonophosphateAdenosine TriphosphateAdenylate KinaseAntineoplastic AgentsArachidonic AcidsarachidonylcyclopropylamideCannabinoidsGlutamineGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)IndolesMorpholinesReactive Oxygen SpeciesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2

Identifiers

PMID23764845
PMCPMC3698539
OpenAlexW2001036106

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.