The therapeutic effect of combined drugs on cervical cancer has been confirmed. Whether antiprogrammed cell death protein 1 antibody combined with paclitaxel mediates the phosphoinositide 3-kinase-protein kinase B pathway to regulate cervical cancer still needs further research. 20 nude mice received subcutaneous administration of Henrietta Lacks cells to establish cervical cancer model which was then assigned into blank control group, control group A (programmed cell death protein 1 antibody (5 mg/ kg) administration), control group B (paclitaxel) and observation group (programmed cell death protein 1 antibody combined with paclitaxel) followed by analysis of cell proliferation, apoptosis, expression of phosphoinositide 3-kinase-protein kinase B signaling related proteins and messenger ribonucleic acids. Observation group had lowest tumor size, highest cell proliferation inhibition rate and cell apoptosis, which were all reversed in blank group with largest tumor size, lowest cell proliferation inhibition rate and cell apoptosis. There was no difference between control group A and control group B (p>0.05). The expressions of phosphoinositide 3-kinase, protein kinase B, tumor protein p53 and tumor protein p21 were lowest in observation group and highest in blank group. In addition, control group had no significant difference with control group B (p>0.05). Anti-programmed cell death protein 1 antibody combined with paclitaxel may inhibit the activity of phosphoinositide 3-kinase-protein kinase B signaling, thereby downregulating phosphoinositide 3-kinase, protein kinase B, tumor protein p53 and tumor protein p21, controlling cervical cancer cell division, promoting cell apoptosis and finally exerting anti-tumor effects.