Gastric Carcinogenesis and Potential Role of the Transient Receptor Potential Vanilloid 1 (TRPV1) Receptor: An Observational Histopathological Study

Author:

Groen Sylvester R.1ORCID,Keszthelyi Daniel1ORCID,Szallasi Arpad2,van Veghel Jara A.1,Alleleyn Annick M. E.1,Csekő Kata345ORCID,Helyes Zsuzsanna345,Samarska Iryna6,Grabsch Heike I.67,Masclee Ad A. M.1,Weerts Zsa Zsa R. M.1

Affiliation:

1. Department of Gastroenterology and Hepatology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center+, 6629 HX Maastricht, The Netherlands

2. Department of Pathology and Experimental Cancer Research, Semmelweis University, 1083 Budapest, Hungary

3. Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, 7624 Pécs, Hungary

4. HUN-REN Chronic Pain Research Group, University of Pécs, 7624 Pécs, Hungary

5. National Laboratory for Drug Research and Development, 1117 Budapest, Hungary

6. Department of Pathology, Maastricht University Medical Center+, 6629 HX Maastricht, The Netherlands

7. Division of Pathology and Data Analytics, Leeds Institute of Medical Research at St James’s University, University of Leeds, Leeds LS2 9JT, UK

Abstract

The potential role of the transient receptor potential Vanilloid 1 (TRPV1) non-selective cation channel in gastric carcinogenesis remains unclear. The main objective of this study was to evaluate TRPV1 expression in gastric cancer (GC) and precursor lesions compared with controls. Patient inclusion was based on a retrospective review of pathology records. Patients were subdivided into five groups: Helicobacter pylori (H. pylori)-associated gastritis with gastric intestinal metaplasia (GIM) (n = 12), chronic atrophic gastritis (CAG) with GIM (n = 13), H. pylori-associated gastritis without GIM (n = 19), GC (n = 6) and controls (n = 5). TRPV1 expression was determined with immunohistochemistry and was significantly higher in patients with H. pylori-associated gastritis compared with controls (p = 0.002). TRPV1 expression was even higher in the presence of GIM compared with patients without GIM and controls (p < 0.001). There was a complete loss of TRPV1 expression in patients with GC. TRPV1 expression seems to contribute to gastric-mucosal inflammation and precursors of GC, which significantly increases in cancer precursor lesions but is completely lost in GC. These findings suggest TRPV1 expression to be a potential marker for precancerous conditions and a target for individualized treatment. Longitudinal studies are necessary to further address the role of TRPV1 in gastric carcinogenesis.

Funder

National Research, Development and Innovation Fund of Hungary

European Union

Publisher

MDPI AG

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