This study investigated the effects of apigenin on endometrial cancer cell proliferation, apoptosis and aerobic glycolysis. The cell viability and cell proliferation of endometrial cancer cells were detected using Cell Counting Kit-8 (CCK8) kit and5-ethynyl-2′-deoxyuridine (EDU) staining. Flow cytometry analysis was used to detect the rate of apoptosis in endometrial cancer cells. Lactate production, glucose consumption, and Adenosine triphosphate (ATP) levels were also measured. Western blot was used to detect the expression of Bcl2-Associated X (BAX), B-cell lymphoma 2 (BCL-2), Cleaved Caspase-3, phosphoinositide 3-kinase (PI3K), p-PI3K, rapamycin (mTOR), p-mTOR, Phosphatase and tensin homolog (PTEN), protein kinase B (Akt) and p-Akt. The results showed that, apigenin inhibits cell viability, cell proliferation, promotes the rate of apoptosis, and the expression of BAX, Cleaved Caspase-3, and inhibits the expression of BCL-2 of endometrial cancer cells in a dose-dependent manner. In addition, apigenin suppressed lactate production, glucose consumption, and ATP levels and inhibited the phosphorylation of PI3K and Akt in a dose-dependent manner. Finally, apigenin inhibited the proliferation and aerobic glycolysis of endometrial cancer cells and promoted cell apoptosis by blocking the PI3K/Akt signaling pathway.