GPR43 Suppresses Intestinal Tumor Growth by Modification of the Mammalian Target of Rapamycin Complex 1 Activity in ApcMin/+ Mice.
Med Princ Pract
; 31(1): 39-46, 2022.
Article
en En
| MEDLINE
| ID: mdl-34818236
ABSTRACT
OBJECTIVE:
G protein-coupled receptor 43 (GPR43), a receptor for short-chain fatty acids, plays a role in suppressing tumor growth; however, the detailed underlying mechanism needs to be comprehensively elucidated. In this study, we investigated the role of GPR43 in inhibiting tumor growth using ApcMin/+, a murine model of intestinal tumors. MATERIALS ANDMETHODS:
Using GPR43-/- ApcMin/+ and GPR43+/- ApcMin/+ mice, the number of tumors was analyzed at the end of the experimental period. Immunohistochemistry, quantitative polymerase chain reaction, and Western blotting were performed to analyze cellular proliferation and proliferation-associated signal pathways.RESULTS:
Our results revealed that GPR43 deficiency resulted in increased tumor numbers in ApcMin/+ mice. Ki67 was highly expressed in GPR43-/- mice (p > 0.05). Increased expression levels of proinflammatory cytokines, including interleukin-6 and tumor necrosis factor-α, and amino acid transporters were not observed in GPR43-deficient mice compared to GPR43-sufficient mice. Furthermore, GPR43-deficient tumor tissues showed enhanced mammalian target of rapamycin-mediated phosphorylated ribosomal protein S6 kinase beta-1 (p > 0.05) and phosphorylated eukaryotic translation initiation factor 4E-binding protein 1 (p > 0.05), but not Akt (protein kinase B) phosphorylation (p = 0.7088).CONCLUSION:
Collectively, GPR43 affords protection against tumor growth at least partly through inhibition of the mammalian target of rapamycin complex 1 pathway.Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Receptores Acoplados a Proteínas G
/
Ácidos Grasos Volátiles
/
Neoplasias Intestinales
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Med Princ Pract
Asunto de la revista:
EDUCACAO
Año:
2022
Tipo del documento:
Article
País de afiliación:
Japón