Mongolian Journal of Health Sciences 2025;88(4):52-55

Study on the anticancer effect of apigenin on leukemia cells

Erdenezaya O 1 ; Enkhkhishig O 2 ; Egshiglen A 3 ; Ulziisaikhan B 3 ; Nomiungerel R 4 ; Enkhmaa D 5 ; Uugangerel E 5

Affiliations

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Keywords

RAW264.7; Flow cytometry; Apigenin-7-O-glycoside; Anticancer; Cell viability

Country

Mongolia

Language

Mongolian

Abstract

Background:The study of small-molecule compounds with antitumor activity involves several crucial steps. These include determining their selective effects on cancer cells, understanding the type of cell death they induce, identifying the activated signaling pathways, pinpointing the target molecules, and elucidating the mechanisms of action. Among the plant-derived compounds with anticancer properties, flavonoids are notable for their ease of isolation and their abundance in food. Apigetrin, a representative flavonoid, is a secondary metabolite found in plants, and our previous study indicated that its anticancer selectivity index was 13.1. However, the specific mechanism by which apigetrin inhibits leukemia cell growth remains unclear.

Aim:To study of the inhibitory action of apigenin on leukemia cell culture

Materials and Methods:In this study, we evaluated the apoptosis of cells using flow cytometry and investigated the in volvement of the caspase pathway through the use of pancaspase inhibitors to explore the effects of apigetrin on leukemia cell growth.

Results:After incubating leukemia RAW264.7 cells with 30 μM apigetrin for 24 and 48 hours, we did not detect any apoptosis through Annexin V and PI staining by flow cytometry. We compared the number of viable cells using the MTT assay after 24-hour treatment of apigetrin with or without pretreatment of Z-VAD, a pancaspase inhibitor, for 30 minutes. The results indicated that the pancaspase inhibitor did not reduce the inhibitory effect of apigetrin on the growth of RAW264.7 cells. In contrast, the positive control group, treated with doxorubicin—which induces apoptosis—showed not only significant apoptosis but also a reduction of the pancaspase inhibitor on the cell growth inhibition. Therefore, these data suggested that apigetrin likely has a cytostatic effect or inhibits the cell cycle rather than being cytotoxic. Future research should focus on determining which stage of the cell cycle RAW264.7 cells treated with apigetrin are in, as well as studying the signaling pathways involved in the cell cycle.

Conclusions:Apigetrin inhibits the proliferation of RAW264.7 leukemia cells in a caspase-independent and non-apoptotic manner.