Evidence map›Paper›PMID 22594963›Full record

ArticleBritish journal of pharmacology2013

Non-THC cannabinoids inhibit prostate carcinoma growth in vitro and in vivo: pro-apoptotic effects and underlying mechanisms.

Luciano De Petrocellis, Alessia Ligresti, Aniello Schiano Moriello, Mariagrazia Iappelli, Roberta Verde, Colin G Stott, Luigia Cristino, Pierangelo Orlando, Vincenzo Di Marzo

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 2 pooled it
4.9field-weighted citation impact, top 5% 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

108 citing papers in PubMed, 2 syntheses or guidelines pooled it, 200 citations in OpenAlex.

  1. Pooled it
  2. Cannabinoids and Prostate Cancer: A Systematic Review of Animal Studies.International journal of molecular sciences · 2020
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  8. Randomized and Blind Evaluation of the Efficacy of a Full-Spectrum OralAnimals : an open access journal from MDPI · 2026
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48 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Luciano De PetrocellisIstituto di Cibernetica, Endocannabinoid Research Group, Consiglio Nazionale delle Ricerche, Pozzuoli, Italy. l.depetrocellis@cib.na.cnr.it
Alessia Ligresti
Aniello Schiano Moriello
Mariagrazia Iappelli
Roberta Verde
Colin G Stott
Luigia Cristino
Pierangelo Orlando
Vincenzo Di Marzo
Istituto di Cibernetica “Eduardo Caianiello” · ITIstituto di Chimica Biomolecolare · ITGW Pharmaceuticals (United Kingdom) · GBInstitute of Protein Biochemistry · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeCannabinoid receptor activation induces prostate carcinoma cell (PCC) apoptosis, but cannabinoids other than Δ(9) -tetrahydrocannabinol (THC), which lack potency at cannabinoid receptors, have not been investigated. Some of these compounds antagonize transient receptor potential melastatin type-8 (TRPM8) channels, the expression of which is necessary for androgen receptor (AR)-dependent PCC survival. EXPERIMENTAL APPROACH: We tested pure cannabinoids and extracts from Cannabis strains enriched in particular cannabinoids (BDS), on AR-positive (LNCaP and 22RV1) and -negative (DU-145 and PC-3) cells, by evaluating cell viability (MTT test), cell cycle arrest and apoptosis induction, by FACS scans, caspase 3/7 assays, DNA fragmentation and TUNEL, and size of xenograft tumours induced by LNCaP and DU-145 cells. KEY

resultsCannabidiol (CBD) significantly inhibited cell viability. Other compounds became effective in cells deprived of serum for 24 h. Several BDS were more potent than the pure compounds in the presence of serum. CBD-BDS (i.p.) potentiated the effects of bicalutamide and docetaxel against LNCaP and DU-145 xenograft tumours and, given alone, reduced LNCaP xenograft size. CBD (1-10 µM) induced apoptosis and induced markers of intrinsic apoptotic pathways (PUMA and CHOP expression and intracellular Ca(2+)). In LNCaP cells, the pro-apoptotic effect of CBD was only partly due to TRPM8 antagonism and was accompanied by down-regulation of AR, p53 activation and elevation of reactive oxygen species. LNCaP cells differentiated to androgen-insensitive neuroendocrine-like cells were more sensitive to CBD-induced apoptosis. CONCLUSIONS AND IMPLICATIONS: These data support the clinical testing of CBD against prostate carcinoma.

Indexed as

Androgen AntagonistsAnilidesAnimalsApoptosisCannabidiolCannabinoidsCaspase 3Cell CycleCell SurvivalDocetaxelDown-RegulationDronabinolDrug InteractionsHumansMaleMiceAndrogen AntagonistsAnilidesbicalutamideCannabidiolCannabinoidsCaspase 3DocetaxelDronabinolNitrilesReactive Oxygen SpeciesReceptors, AndrogenTaxoidsTosyl CompoundsTransient Receptor Potential ChannelsTRPM8 protein, humanTRPM Cation Channels

Identifiers

PMID22594963
PMCPMC3570006
OpenAlexW1485494169

What OpenQuestion holds

Textmetadata
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.