MDMX reprograms glycolysis of hepatocellular carcinoma via 14-3-3γ/FOXO1

8.5
来源: Nature 关键字: mRNA
发布时间: 2025-11-08 03:47
摘要:

MDMX plays a crucial role in hepatocellular carcinoma (HCC) by promoting glycolysis through the degradation of FOXO1, a key tumor suppressor. The study demonstrates that MDMX is overexpressed in HCC tissues, correlating with poor patient prognosis, particularly in those with mutant p53. Mechanistically, MDMX enhances the interaction between FOXO1 and 14-3-3γ, leading to FOXO1 degradation and subsequent metabolic reprogramming. These findings suggest that targeting MDMX could provide new therapeutic strategies for HCC treatment.

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关键证据

MDMX is overexpressed in HCC and correlates with poor prognosis.
MDMX promotes glycolysis by degrading FOXO1, enhancing glucose uptake and lactate production.
Transgenic mouse models confirm MDMX's role in metabolic reprogramming in HCC.

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MDMX plays a crucial role in hepatocellular carcinoma (HCC) by promoting glycolysis through the degradation of FOXO1, a key tumor suppressor. The study demonstrates that MDMX is overexpressed in HCC tissues, correlating with poor patient prognosis, particularly in those with mutant p53. Mechanistically, MDMX enhances the interaction between FOXO1 and 14-3-3γ, leading to FOXO1 degradation and subsequent metabolic reprogramming. These findings suggest that targeting MDMX could provide new therapeutic strategies for HCC treatment.

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