Mechanism by which Human Papillomavirus 16 Infection Interferes with Progression and Immune Evasion of Cervical Cancer by Acting on Th9 Cytokines

High-risk human papillomavirus types are associated with most of cervical cancer cases. To explore the mechanism by which human papillomavirus 16 infections interferes with the progression and immune evasion of cervical cancer by acting on T helper 9 cells cytokines. Cervical cancer cells were obtained from China Center for Type Culture Collection. Cells were cultured in Roswell Park Memorial Institute Medium-1640. Through wound healing test and transwell analysis, the effect of interleukin-9 on the movement, migration and invasion of cancer cells was evaluated. The expression of epithelial-mesenchymal transition markers and programmed death-ligand 1 and programmed cell death protein 1 messenger ribonucleic acid was detected. Human papillomavirus 16 and interleukin-9 receptor had higher expression in cervical cancer tumor tissue than normal group. The proliferation of cervical cancer cells was inhibited in interleukin-9 transfection group compared with the cervical cancer group. Interleukin-9 transfection group reduced N-cadherin and vimentin expression, and increased E-cadherin expression. Interleukin-9 inhibition group increased N-cadherin and vimentin expression and decreased E-cadherin expression. Interleukin-9 transfection group reduced programmed death-ligand 1 and programmed cell death protein 1 expression, while interleukin-9 inhibition group increased programmed death-ligand 1 and programmed cell death protein 1 expression. These cytokines can limit tumor proliferation, movement, migration and invasion. They induce the up-regulation of E-cadherin expression in cervical cells and inhibit programmed death-ligand 1 and programmed cell death protein 1 expression, thereby expressing tumor antigens.