Atorvastatin inhibits proliferation and promotes apoptosis of colon cancer cells via COX-2/PGE2/ß-Catenin Pathway.
J BUON
; 26(4): 1219-1225, 2021.
Article
en En
| MEDLINE
| ID: mdl-34564973
ABSTRACT
PURPOSE:
To explore the effects of atorvastatin (ATST) on the proliferation and apoptosis of colon cancer cells through the cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2)/ß-catenin pathway.METHODS:
HCT116 cells were cultured and transfected, and they were treated with ATST at different concentrations for different time. The association between the expressions of COX-2 and PGE2 and the survival time of patients with colon cancer was analyzed via Kaplan-Meier survival analysis. Then the protein expressions of COX-2, ß-catenin and apoptosis-related molecules in HCT116 cells were determined using Western blotting, and the proliferation of HCT116 cells was detected via cell counting kit-8 (CCK-8) assay.RESULTS:
There was a significant difference in the survival rate between HCT116 cells treated with 30 µM ATST and those treated with 0 µM ATST. The survival time was obviously longer in patients with low expressions of COX-2 and PGE2 than that those with high expressions of COX-2 and PGE2. Low expressions of COX-2 and PGE2 in colon cancer tissues indicate a longer survival time. Moreover, a positive correlation was found between HCT116 cell density and COX-2 level, HCT116 cell density and PGE2 level, and COX-2 and PGE2 levels. ATST could down-regulate COX-2 and ß-catenin, and knocking down COX-2 could lower ß-catenin. After treatment with ATST and ATST + anti-COX-2, the activity of cleaved caspase-9, caspase-3 and PARP was remarkably enhanced, suggesting that ATST and ATST + anti-COX-2 can promote apoptosis of HCT116 cells. It was found that ATST and ATST + anti-COX-2 could also inhibit the proliferation of HCT116 cells.
Buscar en Google
Base de datos:
MEDLINE
Asunto principal:
Dinoprostona
/
Apoptosis
/
Neoplasias del Colon
/
Proliferación Celular
/
Ciclooxigenasa 2
/
Beta Catenina
/
Atorvastatina
Idioma:
En
Revista:
J BUON
Asunto de la revista:
NEOPLASIAS
Año:
2021
Tipo del documento:
Article