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Related Experiment Video

Updated: Jun 27, 2026

Serum and Plasma Copy Number Detection Using Real-time PCR

Serum and Plasma Copy Number Detection Using Real-time PCR

Published on: December 15, 2017

CNR1 and CNR2 Cannabinoid Receptor Mutations in Cancer Cells.

Lillian Schneider¹, Maria Ruano¹, Camryn R Mackey¹

¹Biology Undergraduate Program, The Ohio State University, Marion, OH 43302, USA.

Current Issues in Molecular Biology

|June 26, 2026

Summary

Mutations in cannabinoid receptors CNR1 and CNR2 were analyzed in cancer. Most mutations appear to deactivate these genes, suggesting they are not driver genes in cancer development.

Keywords:

cancer cannabinoid receptors genetic mutation

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Area of Science:

Molecular Biology
Genetics
Cancer Research

Background:

Cannabinoids, such as THC and CBD, interact with the endocannabinoid system.
Key receptors in this system are CNR1 and CNR2, which are G-protein-coupled receptors.

Purpose of the Study:

To map and analyze mutations in CNR1 and CNR2 using the COSMIC database.
To identify mutation trends and signatures in these cannabinoid receptors.

Main Methods:

Utilized the Catalogue of Somatic Mutations in Cancers (COSMIC) database.
Performed in silico 3D structure analysis of mutated proteins.
Analyzed mRNA expression levels of CNR1 and CNR2 across various cancer types.

Main Results:

Identified several mutations in both CNR1 and CNR2.
Mutations were found to cluster in intracellular regions, potentially destabilizing G-protein interactions.
CNR1 and CNR2 showed normal mRNA expression, with a tendency for overexpression in kidney cancer.
Neither CNR1 nor CNR2 were identified as driver genes; mutations resulted in loss of function.

Conclusions:

Somatic mutations in CNR1 and CNR2 are likely deactivating, indicating a loss of function in cancer cells.
These receptors do not appear to be driver genes in cancer development.