Garcinol inhibits the proliferation of endometrial cancer cells by inducing cell cycle arrest.
Oncol Rep
; 45(2): 630-640, 2021 02.
Article
de En
| MEDLINE
| ID: mdl-33416149
ABSTRACT
Endometrial cancer (EC) is the most common gynecological cancer, and one of the most important causes of cancerrelated deaths in women worldwide. The longterm survival rate is lower in advancedstage and recurrent EC, therefore it is important to identify new anticancer drugs. Garcinol, a polyisoprenylated benzophenone, is a promising anticancer drug for various cancer types but its effects on EC remain unclear. To investigate the anticancer effects of garcinol on EC, cell proliferation and cell cycle were assessed by realtime cell proliferation, cell counting, and colony formation assays, flow cytometric analysis, and 5ethynyl2'deoxyuridine (EdU) incorporation assay, in EC Ishikawa (ISH) and HEC1B cell lines. Western blotting was used to evaluate the expression of cell cyclerelated protein cyclins, cyclindependent kinase and tumor suppression proteins. Garcinol inhibited ISH and HEC1B cell proliferation in a dosedependent manner, and induced ISH and HEC1B cell cycle arrest at the G1 phase and G2/M phase, respectively, and decreased the S phase and DNA synthesis in these two cell lines. Following garcinol treatment the expression levels of p53 and p21 were increased, while the expression levels of CDK2, CDK4, cyclin D1 and cyclin B1 were gradually decreased in a dosedependent manner in both ISH and HEC1B cells. In addition, the expression levels of phosphorylated cJUN Nterminal kinase (JNK) and pcJUN were significantly increased in both types of cells. Collectively, garcinol can induce EC cell cycle arrest and may be a promising candidate for EC chemotherapy.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Terpènes
/
Tumeurs de l'endomètre
/
Points de contrôle de la phase G2 du cycle cellulaire
Limites:
Female
/
Humans
Langue:
En
Journal:
Oncol Rep
Sujet du journal:
NEOPLASIAS
Année:
2021
Type de document:
Article