Background: Ovarian cancer is the second leading cause of death in Iran compared with other gynecological diseases. Considering the role of cyclooxygenase (COX) enzymes and prostaglandin E2 production in tumor lesions, nonsteroidal anti-inflammatory drugs (NSAIDs) show antitumor properties by inhibiting COX. Furthermore, some compounds can serve as non-selective inhibitors of COX (such as ketoprofen) and prevent cancer development. Human epididymis protein 4 (HE4) is one of the most sensitive tumor markers known in the study of the disease of ovarian epithelial cancer. The expression of HE4 increases in different types of ovarian cancer. Objectives: The aim of this study was to determine the anti-cancer effects of ketoprofen on the viability of ovarian cancer cells and expression of HE4 gene. Methods: To calculate half-maximal inhibitory concentration (IC50), A2780S cells were treated with different concentrations of ketoprofen for 24 hours, then the cells were incubated with appropriate concentrations of IC50 for 24, 48, and 72 hours. Real-time polymerase chain reaction (PCR) was used to measure changes caused by the effect of drugs on HE4 gene expression and analyzed by the 2-ΔΔCT method. Results: The IC50 level of ketoprofen for 24 hours was 583.7 μM. According to real-time PCR results, treatment of cells with ketoprofen reduced HE4 expression. Conclusions: HE4 gene expression decreased in cells treated with ketoprofen compared with the cells in the control group, which proves the anti-cancer activity of ketoprofen and a reduction in the viability of ovarian cancer cells.
Introduction: Ovarian cancer is one of the deadliest genital cancers among females and mainly originates from epithelial cells. The cancer generally remains asymptomatic until metastasis. Silibinin, a derivative of Silybum marianum, is a flavonoid with anticancer effects against many tumor cells. The sortilin1 (SORT1) gene has been shown to be overexpressed in ovarian tumors. Here, we investigated the effects of silibinin on SORT1 gene expression and the viability of ovarian A2780s cancer cell line.Methods: The A2780s ovarian cancer cell line was treated with silibinin at the concentrations of 50, 100, and 200 μM for 24 hours, and IC50 (half-maximal inhibitory concentration) was determined. Then the viability percentage of the cells treated with 100 μM silibinin was determined at 24, 48, and 72 hours. After 24 and 48 hours exposure to 100 μM silibinin, RNA was extracted, followed by cDNA synthesis and SORT1 gene expression analysis using glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as the reference gene by real-time Polymerase chain reaction (PCR).Results: Silibinin in a dose- and time-dependent manner reduced the viability of ovarian cancer cells (P < 0.05), accompanied by a reduction in SORT1 gene expression.Conclusion: The present study showed that silibinin had toxic effects against the A2780s ovarian cancer cell line, suggesting this compound as a potential anticancer agent.
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