Journal
ONCOIMMUNOLOGY
Volume 7, Issue 1, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/2162402X.2017.1375640
Keywords
autophagy; colitis-associated colorectal cancer; colitis; GL-V9; NLRP3 inflammasome
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Funding
- National Science & Technology Major Project [2012ZX09304-001, 2013ZX09103-001-007]
- Program for Changjiang Scholars and Innovative Research Team in University [IRT1193]
- National Natural Science Foundation of China [91029744, 81373448, 81373449]
- Project Program of State Key Laboratory of Natural Medicines, China Pharmaceutical University [SKLNMZZCX201606]
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Emerging evidence suggests that NLRP3 inflammasome provides a link between colitis-associated colorectal cancer and inflammatory bowel diseases. Autophagy is induced in macrophages by AMPK activation and regulates NLRP3 inflammasome to maintain intracellular homeostasis. Here we report that a small-molecule AMPK activator (GL-V9) exerts potent anti-inflammatory effects on macrophages invitro and in vivo, which trigger autophagy to degraded NLRP3 inflammasome. Treatment with GL-V9 protected against colitis and tumorigenesis in colitis-associated colorectal cancer. This suggests that GL-V9 may be an interesting candidate for clinical evaluation in the treatment of colitis-associated colorectal cancer.
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