Disruption of the endocannabinoid system is prominent in lung adenocarcinoma and associated with poor patient survival

Kelsie Thu,Roland Hubaux,Wan Lam,Stephen Lam

doi:10.1186/2049-3002-2-s1-p76

Abstract

Background The endocannabinoid system (ECS) is comprised of cannabinoid receptors, lipid messengers called endocannabinoids, and the enzymes that metabolize them. It modulates numerous processes including the central nervous and immune systems as well as cell signaling pathways important in normal function and diseases such as cancer. Many studies have demonstrated anti-tumour effects of synthetic and endogenous cannabinoids in cancer, emphasizing the potential for ECS modulators as anti-cancer therapies. We believe that ECS deregulation may contribute to the malignant phenotype of lung cancer cells by reducing anti-tumour endocannabinoid levels and consequently increasing levels of arachidonic acid, which can promote tumour growth. We sought to determine whether the ECS is disrupted in clinical lung tumours and whether disruption has prognostic implications.

Highlights

The endocannabinoid system (ECS) is comprised of cannabinoid receptors, lipid messengers called endocannabinoids, and the enzymes that metabolize them
Disruption of the endocannabinoid system is prominent in lung adenocarcinoma and associated with poor patient survival
The ECS was recurrently disrupted in both lung adenocarcinoma cohorts; 78% and 82% of tumours in the BCCA (n=83) and TCGA (n=57) cohorts, respectively, harboured gene expression changes consistent with our hypothesis in at least one of the five components assessed

Summary

Introduction

The endocannabinoid system (ECS) is comprised of cannabinoid receptors, lipid messengers called endocannabinoids, and the enzymes that metabolize them. It modulates numerous processes including the central nervous and immune systems as well as cell signaling pathways important in normal function and diseases such as cancer. Many studies have demonstrated anti-tumour effects of synthetic and endogenous cannabinoids in cancer, emphasizing the potential for ECS modulators as anti-cancer therapies. We believe that ECS deregulation may contribute to the malignant phenotype of lung cancer cells by reducing anti-tumour endocannabinoid levels and increasing levels of arachidonic acid, which can promote tumour growth. We sought to determine whether the ECS is disrupted in clinical lung tumours and whether disruption has prognostic implications

Methods

Results

Conclusion