Activation of STING inhibits cervical cancer tumor growth through enhancing the anti-tumor immune response.

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+ T cell and CD103+ dendritic cell numbers. The NF-κB signal inhibitor limited the increasing numbers of CD8+ T cell and CD103+ dendritic cells induced by ADU-S100, without influence on tumor growth. Hence, our study suggested that STING could serve as a potential novel immunotherapeutic target for cervical cancer. PMID: 33141310 [PubMed - as supplied by publisher]
Source: Molecular and Cellular Biochemistry - Category: Biochemistry Authors: Tags: Mol Cell Biochem Source Type: research