Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2026
Curcumin inhibits colorectal cancer progression by regulating MDH2-mediated glycolysis and NAD+ metabolism.
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Zhao Yuwei, Qin Hao, Sun Wei, Chen Yu, Wang Ruoyu, Li Chuang
Аннотация
INTRODUCTION: Abnormal glycolysis drives colorectal cancer (CRC) progression. Curcumin (Cur) has anti-CRC activity, but its effect on glycolysis remains unclear. This study explores Cur's regulation of glycolysis in CRC cells.
METHODS: Using SW480 and HCT-116 cells, bioinformatics identified key targets. MDH2 was knocked down via shRNA. Effects of Cur alone or with 2-DG on proliferation were assessed by CCK-8 and Transwell assays. Glycolytic indicators and protein levels were measured using kits and Western blotting. In vivo validation used CRC xenograft mice.
RESULTS: Cur dose-dependently inhibited CRC cell glycolysis, reducing metabolic indicators and downregulating key proteins/NAD+/NADH ratio. Cur combined with 2-DG synergistically suppressed glycolysis and cell proliferation. Bioinformatics showed higher MDH2 expression in CRC tissues (enriched in glycolysis). MDH2 knockdown enhanced Cur's anti-tumor effects and glycolysis suppression in vitro. In vivo, MDH2 silencing potentiated Cur's tumor-inhibitory efficacy, with reduced tumor size, increased necrosis, and enhanced downregulation of glycolytic/NAD+ metabolic proteins.
CONCLUSIONS: The study systematically demonstrated that curcumin suppresses CRC progression by targeting the MDH2-driven glycolysis and NAD+ metabolic axis, thereby providing novel theoretical basis for metabolism-targeted CRC therapies.
METHODS: Using SW480 and HCT-116 cells, bioinformatics identified key targets. MDH2 was knocked down via shRNA. Effects of Cur alone or with 2-DG on proliferation were assessed by CCK-8 and Transwell assays. Glycolytic indicators and protein levels were measured using kits and Western blotting. In vivo validation used CRC xenograft mice.
RESULTS: Cur dose-dependently inhibited CRC cell glycolysis, reducing metabolic indicators and downregulating key proteins/NAD+/NADH ratio. Cur combined with 2-DG synergistically suppressed glycolysis and cell proliferation. Bioinformatics showed higher MDH2 expression in CRC tissues (enriched in glycolysis). MDH2 knockdown enhanced Cur's anti-tumor effects and glycolysis suppression in vitro. In vivo, MDH2 silencing potentiated Cur's tumor-inhibitory efficacy, with reduced tumor size, increased necrosis, and enhanced downregulation of glycolytic/NAD+ metabolic proteins.
CONCLUSIONS: The study systematically demonstrated that curcumin suppresses CRC progression by targeting the MDH2-driven glycolysis and NAD+ metabolic axis, thereby providing novel theoretical basis for metabolism-targeted CRC therapies.