STING promotes proliferation and induces drug resistance in colorectal cancer by regulating the AMPK mTOR pathway

Abstract Background: Despite a rapidly growing body of pertinent literature, what role the protein stimulator of interferon genes (STING) plays in colorectal cancer (CRC) remains unclear. We are committed to exploring whether STING can be adopted as an effective target and biomarker for CRC. Methods: STING expression was examined by immunohistochemistry to evaluate its association with clinicopathological factors. In addition, the effects of STING on various biological characteristics of CRC cells, such as proliferation, migration, invasiveness and drug resistance, were also studied. Gene set enrichment analysis was an indispensable tool to study the downstream mechanism of STING. Meanwhile, we explored the effect of STING on glucose uptake. Results: Our study suggested that the expression of STING was not only up-regulated in CRC, but also correlated with TNM stage and poor prognosis. Moreover, STING regulates cell migration, proliferation, invasiveness and drug resistance via mediating AMPK-mTOR pathway. Finally, we confirmed that STING regulates energy metabolism in CRC cells. Conclusions: STING may be a promising biomarker and a target for chemosensitization and inhibition of CRC progression.