Apigenin induces apoptosis and reverses the drug resistance of ovarian cancer cells

Objective: Ovarian cancer is one of the most common malignant tumors in the female reproductive system and one of the most common gynecological diseases in the world. Its incidence has been increasing in recent years. Apigenin, an inexpensive drug, has few adverse reactions and significant anti-inflammatory, antiviral, and oxidative effects. If it can be applied to the treatment of ovarian cancer, it will have a great significance for future clinical treatment. The study examines the effect of Apigenin on apoptosis and the reversal of ovarian cancer cell drug resistance by regulating Mcl-1. Methods: The ovarian cancer-sensitive cell line SKOV3 and the ovarian cancer drug resistant cell line SKOV3/DDP were used as experimental samples. The ovarian cancer-sensitive cell line SKOV3 was divided into sensitive A (SKOV3+apigenin) with apigenin intervention, sensitive B (DPP+SKOV3) with DPP intervention, and sensitive C (apigenin+DDP+SKOV3) with apigenin and cisplatin (DDP) intervention. Similarly, the ovarian cancer drug resistant cell line SKOV3/DDP was divided into drug resistant A (SKOV3/DDP+apigenin), drug resistant B (SKOV3/DDP+DPP), and drug resistant C (SKOV3/DDP+DDP+SKOV3). The cell proliferation was tested using MTT in each group. The cell apoptosis in each group was tested using flow cytometry. The RNA and protein expressions of Mcl-1 were tested in each group. The anti-tumor effects of apigenin on the sensitive cell line and the drug resistant cell line were observed, as was the effects on the sensitivity of the various cell lines to the chemotherapeutic drug DDP. Results: There was no significant difference in the proliferation of cancer cells between sensitive A and sensitive B (P>0.050). The proliferation of sensitive C was significantly lower than the proliferation of sensitive A and sensitive B (P<0.050). There was no significant difference in the apoptosis between sensitive A and sensitive B (P>0.050). The apoptosis of sensitive C was significantly higher than the apoptosis of sensitive A and sensitive B (P<0.050). The cell proliferation in drug resistant A was significantly lower than it was in drug resistant B (P<0.050), and lower than it was in drug resistant C (P<0.001). There was no significant difference in apoptosis between drug resistant B and drug resistant C (P<0.050). The apoptosis of drug resistant A was significantly higher than the apoptosis of drug resistant B and C. Conclusion: Apigenin can enhance the chemosensitivity of ovarian cancer sensitive cells and drug resistant cells. The mechanism may work by inducing the apoptosis of ovarian cancer cells by down-regulating the Mcl-1 gene.