Activation of STING inhibits cervical cancer tumor growth through enhancing the anti-tumor immune response
Cervical cancer remains the second leading cause of gynecologic cancer-related mortality among women worldwide. STING (stimulator of interferon genes) was reported to be involved in the immune surveillance of tumors. However, the specific role of STING in cervical cancer remains unclear. In this study, we found that the cGAS (Cyclic GMP-AMP synthase)/STING signal decreased in cervical cancer cells. Knockdown of STING by siRNA enhanced the cell viability and migration of cervical cancer cells, while activation of STING by ADU-S100 inhibited the cell viability of cervical cancer cells, with no effect on the migration and apoptosis. In addition, ADU-S100 promoted the secretion of IFNβ and IL-6, and the activation of TBK1 (TANK-binding kinase 1)/NF-κB (nuclear factor kappa-B) pathway. Meanwhile, knockdown of STING inhibited the production of IFNβ and IL-6 that were triggered by dsDNA and suppressed the TBK1/NF-κB signaling. ADU-S100 also suppressed tumor growth in vivo and increased the tumor-infiltrating CD8
