Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid Stoffw Microb

Hasenoehrl, C; Feuersinger, D; Sturm, EM; Bärnthaler, T; Heitzer, E; Graf, R; Grill, M; Pichler, M; Beck, S; Butcher, L; Thomas, D; Ferreirós, N; Schuligoi, R; Schweiger, C; Haybaeck, J; Schicho, R.
G protein-coupled receptor GPR55 promotes colorectal cancer and has opposing effects to cannabinoid receptor 1.
Int J Cancer. 2018; 142(1):121-132 Doi: 10.1002/ijc.31030 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Führende Autor*innen der Med Uni Graz
Hasenöhrl Carina
Schicho Rudolf
Co-Autor*innen der Med Uni Graz
Bärnthaler Thomas
Böhm Eva
Graf Ricarda
Grill Magdalena
Haybäck Johannes
Heitzer Ellen
Pichler Martin
Schuligoi Rufina

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

The putative cannabinoid receptor GPR55 has been shown to play a tumor-promoting role in various cancers, and is involved in many physiological and pathological processes of the gastrointestinal (GI) tract. While the cannabinoid receptor 1 (CB1 ) has been reported to suppress intestinal tumor growth, the role of GPR55 in the development of GI cancers is unclear. We, therefore, aimed at elucidating the role of GPR55 in colorectal cancer (CRC), the third most common cancer worldwide. Using azoxymethane (AOM)- and dextran sulfate sodium (DSS)-driven CRC mouse models, we found that GPR55 plays a tumor-promoting role that involves alterations of leukocyte populations, i.e. myeloid-derived suppressor cells and T lymphocytes, within the tumor tissues. Concomitantly, expression levels of COX-2 and STAT3 were reduced in tumor tissue of GPR55 knockout mice, indicating reduced presence of tumor-promoting factors. By employing the experimental CRC models to CB1 knockout and CB1 /GPR55 double knockout mice, we can further show that GPR55 plays an opposing role to CB1 . We report that GPR55 and CB1 mRNA expression are differentially regulated in the experimental models and in a cohort of 86 CRC patients. Epigenetic methylation of CNR1 and GPR55 was also differentially regulated in human CRC tissue compared to control samples. Collectively, our data suggest that GPR55 and CB1 play differential roles in colon carcinogenesis where the former seems to act as oncogene and the latter as tumor suppressor. © 2017 UICC.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Carcinogenesis - metabolism
Colorectal Neoplasms - metabolism
Colorectal Neoplasms - pathology
Humans -
Mice -
Mice, Knockout -
Receptor, Cannabinoid, CB1 - metabolism
Receptors, Cannabinoid - metabolism
Receptors, G-Protein-Coupled - metabolism

Find related publications in this database (Keywords)
colorectal carcinogenesis
© Med Uni Graz Impressum