Fig. 1From: An integrated approach of network pharmacology, molecular docking, and experimental verification uncovers kaempferol as the effective modulator of HSD17B1 for treatment of endometrial cancerKaempferol suppressed the proliferation, promoted apoptosis, and limited the tumor-forming, invasion, and migration capacities of both ER-subtype human endometrial cancer cells. A Kaempferol inhibited human endometrial cancer cells' proliferation (ER-positive AN3 CA and Ishikawa, ER-negative HEC-1-A and HEC-1-B EC cells) in a dose- and time-dependent manner. B The IC50 values of kaempferol at 48 h were 6.38, 24.35, 35.62, 38.31, 69.87, 104.90, 266.10, and 383.60 μg·mL−1 for AN3 CA, Ishikawa, HEC-1-A, HEC-1-B, CCD 841 CoN, WRL 68, MRC-5 and human monocytes, respectively. C–D Kaempferol significantly inhibited AN3 CA cell colony formation in a dose-dependent manner. E The early apoptotic cells and late-stage apoptotic cells of EC cells (AN3 CA, Ishikawa, HEC-1-A, and HEC-1-B) were both increased after treatment with kaempferol in a dose-dependent manner. F Kaempferol induced cell apoptosis by elevating the expression of cleaved CASP3 and cleaved CASP9 in a dose-dependent manner. G Kaempferol inhibited EC cells’ wound healing in a time- and dose-dependent manner. In a concentration-dependent manner, kaempferol inhibited migration H–I and invasion J–K. The results are presented as means and standard deviations (SDs) from triplicate experiments. Kae: Kaempferol; Compared with the negative control, *, #P < 0.05, **, ##P < 0.01, ***, ###P < 0.001Back to article page