〔Abstract〕 Objective To investigate the effect of quinalizarin on cervical cancer Caski cells. Methods Human cervical carcinoma Caski cells were culturedin vitroand pretreated with quinalizarin culture medium at different concentrations(0, 1, 4, 12 μmol/L), 5-fluorouracil group(5 μmol/L) as a positive control. The proliferation of Caski cells was detected by BrdU staining; the apoptosis of Caski cells was detected by flow cytometry; the microtubule-associated protein 1 light chain 3(LC3)content was detected by immunofluorescence; the expression of phosphorylation-related proteins in proliferation, apoptosis, autophagy and PI3 K pathway was detected by Western blot; CaSki cells were injected into nude mice to construct model with the transplanted tumor and verifiedin vivo. Results Compared with the control group(0 μmol/L), the proliferative capacity of cervical cancer CaSki cells was significantly weakened after treatment with 4 μmol/L and 12 μmol/L quinalizarin, the rate of BrdU positive cells significantly decreased, and the expression of Ki67 protein was also significantly declined. With the increase of quinalizarin concentration, the apoptosis rate of cervical cancer CaSki cells and the expression level of Cleaved caspase-3 gradually increased, and the effect was the most obvious in the 12 μmol/L quinalizarin treatment group. With the increase of the concentration of quinizarin, the expression of ATG5 gradually decreased, the ratio of LC3Ⅱ/LC3Ⅰ and the expression of p62 gradually increased, and the 4 μmol/L and 12 μmol/L quinizarin treatment groups had significant differences compared with the control group. Compared with the treatment with the autophagy inhibitor 3-MA alone, the combined treatment of 3-MA and high concentration(12 μmol/L) quinizarin significantly reversed the inhibitory effect of 3-MA on autophagy and the promotion of 3-MA on the phosphorylation of PI3 K pathway.In vivoexperiments, compared with the control group, the tumor type and weight of the drug-treated group significantly reduced, and their Ki67 and ATG5 expressions significantly reduced, and Caspase-3 expression significantly increased, and the phosphorylation levels of PI3 K, AKT, and mTOR protein significantly reduced, which was consistent with thein vitroexperiments. Conclusion Quinalizarin can inhibit the proliferation of cervical cancer CaSki cells, promote autophagy and apoptosis, possibly by inhibiting the phosphorylation of proteins in PI3 K pathway.