〔Abstract〕 Objective To analyze the induction effect of dendritic cells(DC)-killer cells(CIK) on cervical cancer cell dormancy. Methods Cervical cancer SiHa cells were selected, the venous blood of cervical cancer patients with cervical cancer was collected and peripheral blood mononuclear cell layer was obtained from density gradient centrifugation, DC cells and CIK cells were induced respectively, the effects of DC-CIK cells on cervical cancer SiHa cells survival rate and proliferation, apoptosis, invasion, migration and other biological behavior were observed after group culture, and Western blot method was used for apoptosis and invasive protein expression. Results Compared with cervical cancer group and DC group, CIK group and DC-CIK group had lower proliferation rate and higher apoptosis rate. Compared with CIK group, the proliferation rate of DC-CIK group was lower and the apoptosis rate was higher(P<0.05). Compared with cervical cancer group and DC group, the survival rate of CIK group and DC-CIK group was lower, and the survival rate of DC-CIK group was lower than CIK group(P<0.05). Compared with cervical cancer group and DC group, the number of invading and migrating cells in CIK group and DC-CIK group was lower. Compared with CIK group, the number of invading and migrating cells in DC-CIK group was lower(P<0.05). Compared with cervical cancer group and DC group, the relative expression levels of phosphatidylinositol 3-kinase(PI3 K), protein kinase B(AKT), mammalian target of sirolimus(mTOR), matrix metalloproteinase-9(MMP-9) in CIK group and DC-CIK group were lower, and the relative expression levels of epithelial calcium adhesin(E-cadherin) were higher. Compared with CIK group, the relative expression levels of PI3 K, Akt, mTOR and MMP-9 were lower in DC-CIK group, and the relative expression levels of E-cadherin were higher(P<0.05). Conclusion The establishment of DC-CIK co-culture system and the intervention of cervical cancer cells can inhibit cervical cancer cell proliferation, invasion and migration, and promote cervical cancer cell apoptosis, thus inducing cervical cancer cell dormancy. The mechanism may be related to the use of DC-CIK cell culture to regulate PI3 K/Akt/mTOR pathway protein and invasion-related protein expression.