Objective To investigate the mechanism of aloe emodin (AE) in promoting autophagy by regulating miR-30b expression in endometrial carcinoma cell line HEC-1-B. Methods The expression level of miR-30b in normal endometrial cells and endometrial cancer cell lines HEC-1-A, HEC-1-B, and RL95 - 2 was measured by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR). HEC-1-B cancer cells with the highest expression level of miR-30b were divided into a HEC-1-B cancer cell group, miR-30b inhibitor NC group (transfected with miR-30b inhibitor NC), miR-30b inhibitor group (transfected with miR-30b inhibitor), AE group (30 μmol / L AE, untransfected), AE+ transfection group: AE+miR-30b mimics NC group ( 30 μmol / L AE, transfected with miR-30b mimics NC), and AE+ miR-30b mimics group ( 30 μmol / L AE, transfected with miR-30b mimics). The expression level of miR-30b, cell proliferation, apoptosis rate, and autophagy rate were determined by qRT-PCR, CCK-8 assays, flow cytometry, and monodansulfonyl cadaverine fluorescence staining respectively. Western blot was used to measure the protein expression levels of Beclin 1, LC3-I, LC3-II, and p62. Results Compared with normal human endometrial epithelial cells, expression levels of miR-30b were significantly higher in HEC-1-A, HEC-1-B, and RL95-2 cancer cells (P< 0. 05). The expression level of miR-30b was the highest in HEC-1-B cancer cells. Thus, HEC-1-B cancer cells were selected for transfection experiments. Compared with HEC-1-B cancer cell and miR-30b inhibitor NC groups, the miR-30b inhibitor group had a significantly lower miR-30b expression level, cell proliferation rate, and p62 protein expression level (P< 0. 05), and significantly higher apoptosis rate, autophagy rate, Beclin 1 protein expression level, and LC3-II/ I ratio (P< 0. 05). Compared with the HEC-1-B group, AE and AE+miR-30b mimics NC groups had significantly lower miR-30b expression levels, cell proliferation rates and p62 protein expression levels ( P< 0. 05), and a significantly higher apoptosis rate, autophagy rate, Beclin 1 protein expression level, and LC3-II/ I ratio (P< 0. 05). Compared with the AE+ miR-30b mimics NC group, the AE + miR-30b mimics group had a significantly higher miR-30b expression level, cell proliferation rate, and p62 protein expression level (P< 0. 05), and significantly lower apoptosis rate, autophagy rate, Beclin 1 protein expression level, and LC3-II/ I ratio ( P< 0. 05). Conclusions Expression of miR-30b is high in endometrial carcinoma cells. AE may inhibit the expression of miR-30b, promote autophagy and apoptosis of cancer cells, and inhibit the proliferation of cancer cells. Overexpression of miR-30b reverses the effect of AE.