Background:
Endometrial cancer is a common cause of death in gynecological malignancies. Cisplatin
is a clinically chemotherapeutic agent. However, drug-resistance is the primary cause of treatment failure.
Objective:
Emodin is commonly used clinically to increase the sensitivity of chemotherapeutic agents, yet
whether Emodin promotes the role of Cisplatin in the treatment of endometrial cancer has not been studied.
Method:
CCK-8 kit was utilized to determine the growth of two endometrial cancer cell lines, Ishikawa and
HEC-IB. The apoptosis level of Ishikawa and HEC-IB cells was detected by Annexin V / propidium iodide
double-staining assay. ROS level was detected by DCFH-DA and NADPH oxidase expression. Expressions of
drug-resistant genes were examined by real-time PCR and Western blotting.
Results:
Emodin combined with Cisplatin reduced cell growth and increased the apoptosis of endometrial cancer
cells. Co-treatment of Emodin and Cisplatin increased chemosensitivity by inhibiting the expression of drugresistant
genes through reducing the ROS levels in endometrial cancer cells. In an endometrial cancer xenograft
murine model, the tumor size was reduced and animal survival time was increased by co-treatment of Emodin
and Cisplatin.
Conclusion:
This study demonstrates that Emodin enhances the chemosensitivity of Cisplatin on endometrial
cancer by inhibiting ROS-mediated expression of drug-resistance genes.
The role of surgery in recurrent endometrial cancer