Evidence map›Paper›PMID 27186076›Full record

ArticleBreast cancer (Dove Medical Press)2016

Modulation of breast cancer cell viability by a cannabinoid receptor 2 agonist, JWH-015, is calcium dependent.

Katherine E Hanlon, Alysia N Lozano-Ondoua, Puja J Umaretiya, Ashley M Symons-Liguori, Anupama Chandramouli, Jamie K Moy, William K Kwass, Patrick W Mantyh, Mark A Nelson, Todd W Vanderah

Open access · goldAbstract read
In one paragraph

Article in Breast cancer (Dove Medical Press), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  17. Cannabinoids in the landscape of cancer.Journal of cancer research and clinical oncology · 2021
    Review
  18. Review
  19. Molecular Mechanism of Cannabinoids in Cancer Progression.International journal of molecular sciences · 2021
    Review
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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

10 authors at 1 institution in 1 country.

Katherine E HanlonDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA; Department of Biomedical Sciences, University of New England College of Osteopathic Medicine, Biddeford, ME, USA.
Alysia N Lozano-OndouaDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
Puja J UmaretiyaDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
Ashley M Symons-LiguoriDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
Anupama ChandramouliDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
Jamie K MoyDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
William K KwassDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
Patrick W MantyhDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
Mark A NelsonDepartment of Pathology, University of Arizona College of Medicine, Tucson, AZ, USA.
Todd W VanderahDepartment of Pharmacology, University of Arizona College of Medicine, Tucson, AZ, USA.
University of Arizona · US

Funding

Cannabinoid CB2 Agonists for Treatment of Breast Cancer-Induced Bone PainR01CA142115 · NCI · UNIVERSITY OF ARIZONA · PI VANDERAH, TODD W · 2010 to 2021
$3.3M
NCI NIH HHS R01 CA142115
6 · The paper itself

Abstract

introductionCannabinoid compounds, both nonspecific as well as agonists selective for either cannabinoid receptor 1 (CB1) or cannabinoid receptor 2 (CB2), have been shown to modulate the tumor microenvironment by inducing apoptosis in tumor cells in several model systems. The mechanism of this modulation remains only partially delineated, and activity induced via the CB1 and CB2 receptors may be distinct despite significant sequence homology and structural similarity of ligands.

methodsThe CB2-selective agonist JWH-015 was used to investigate mechanisms downstream of CB2 activation in mouse and human breast cancer cell lines in vitro and in a murine mammary tumor model.

resultsJWH-015 treatment significantly reduced primary tumor burden and metastasis of luciferase-tagged murine mammary carcinoma 4T1 cells in immunocompetent mice in vivo. Furthermore, JWH-015 reduced the viability of murine 4T1 and human MCF7 mammary carcinoma cells in vitro by inducing apoptosis. JWH-015-mediated reduction of breast cancer cell viability was not dependent on Gαi signaling in vitro or modified by classical pharmacological blockade of CB1, GPR55, TRPV1, or TRPA1 receptors. JWH-015 effects were calcium dependent and induced changes in MAPK/ERK signaling.

conclusionThe results of this work characterize the actions of a CB2-selective agonist on breast cancer cells in a syngeneic murine model representing how a clinical presentation of cancer progression and metastasis may be significantly modulated by a G-protein-coupled receptor.

Indexed as

apoptosisbreast cancercalciumcannabinoid receptor-2CB2JWH-015MAPK/ERK

Identifiers

PMID27186076
PMCPMC4847606
OpenAlexW2335971122

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.