Abstract: Objective　To explore the mechanism of Celastrol in inhibiting proliferation and invasion ability of cervical cancer cells.　Methods　Normal cultured HeLa cells were divided into the following groups: a control group, a low-dose Celastrol group, a medium-dose Celastrol group and a high-doses Celastrol group (final concentrations of Celastrol were 4 μmol/L, 8 μmol/L and 12 μmol/L, respectively), a positive control group (cisplatin, final concentration of 10 μmol/L), a LY294002 group (LY294002, final concentration of 20 μmol/L) and a Celastrol with LY294002 group ( final concentrations of Celastrol and LY294002 were 12 μmol/L and 20 μmol/L, respectively). The cell survival conditions of each group were detected by MTT assay. The apoptosis of each group were detected by flow cytometry. The cell invasion of each group were detected by Transwell. The expression of PI3K/AKT/NF-κB signaling pathway were detected by Western Blot. HeLa cells were subcutaneously injected to establish nude mice models to observe the effects of Celastrol (120 mg/kg) on volume and weight of transplanted tumors in nude mice.　Results　Compared with the control group, relative proliferation rate of HeLa cells and number of invasive cells in Celastrol group, positive control group and LY294002 group significantly decreased (P<0.001), while apoptosis rates significantly increased (P<0.001), and expression of p-PI3K, p-AKT and NF-κB p65 protein significantly down-regulated (P<0.001). Moreover, with increasing of Celastrol concentration, its effects increased. Compared with the LY294002 group, relative proliferation rate of HeLa cells and number of invasive cells in the Celastrol with LY294002 group significantly decreased (q=10.182, q=10.217; P<0.001), while apoptosis rate significantly increased (q=23.636, P<0.001). Compared with the control group, weight of nude mice, volume and weight of transplanted tumors of nude mice significantly decreased in the Celastrol groups (q=4.100, P<0.020; q=13.501, P<0.001; q=5.078, P=0.005).　Conclusions　Celastrol may inhibit its malignant biological behaviors through inhibiting the PI3K/Akt/NF-κB signaling pathway of HeLa cells

Key words: Celastrol, 　Cervical cancer, 　PI3K/AKT/NF-κB signaling pathway