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STING promotes proliferation and induces drug resistance via regulating the AMPK-mTOR signaling pathway in colorectal cancer cells
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Abstract
Background: Despite a rapidly growing body of pertinent literature, the relationship between stimulator of interferon genes (STING) protein expression and the progression of colorectal cancer (CRC) remains controversial. This study aimed to investigate the potential roles of STING as a prognostic biomarker and therapeutic target in the medical management of CRC. Methods: STING expression was examined by immunohistochemistry to evaluate its association with clinicopathological factors. Moreover, the effects of STING on CRC cell proliferation, migration, invasiveness, and drug resistance were examined. Gene set enrichment analysis was applied to explore potential downstream mechanisms of STING in CRC. Meanwhile, we evaluated the effect of STING on glucose uptake. Results: Our study confirmed that STING expression was significantly up-regulated in CRC tissues, and was associated with TNM stage and a poor prognosis. Additionally, STING promoted cell proliferation, migration, invasiveness, and drug resistance by mediating AMPK-mTOR signaling. Finally, we confirmed that STING regulates energy metabolism in CRC cells. Conclusions: STING may represent a promising prognostic biomarker and therapeutic target for chemosensitization and inhibition of CRC progression.
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Title: STING promotes proliferation and induces drug resistance via regulating the AMPK-mTOR signaling pathway in colorectal cancer cells
Description:
Abstract
Background: Despite a rapidly growing body of pertinent literature, the relationship between stimulator of interferon genes (STING) protein expression and the progression of colorectal cancer (CRC) remains controversial.
This study aimed to investigate the potential roles of STING as a prognostic biomarker and therapeutic target in the medical management of CRC.
Methods: STING expression was examined by immunohistochemistry to evaluate its association with clinicopathological factors.
Moreover, the effects of STING on CRC cell proliferation, migration, invasiveness, and drug resistance were examined.
Gene set enrichment analysis was applied to explore potential downstream mechanisms of STING in CRC.
Meanwhile, we evaluated the effect of STING on glucose uptake.
Results: Our study confirmed that STING expression was significantly up-regulated in CRC tissues, and was associated with TNM stage and a poor prognosis.
Additionally, STING promoted cell proliferation, migration, invasiveness, and drug resistance by mediating AMPK-mTOR signaling.
Finally, we confirmed that STING regulates energy metabolism in CRC cells.
Conclusions: STING may represent a promising prognostic biomarker and therapeutic target for chemosensitization and inhibition of CRC progression.
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