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Aldolase B suppresses hepatocellular carcinogenesis by inhibiting G6PD and pentose phosphate pathways

Min Li1,2, Xuxiao He1,2, Weixing Guo3

  • 1CAS Key Laboratory of Nutrition, Metabolism and Food Safety Research, Shanghai Institute of Nutrition and Health (SINH), Chinese Academy of Sciences (CAS), Shanghai, China.

Nature Cancer
|February 5, 2022
PubMed

Insights

Hepatic aldolase B (Aldob) suppresses liver cancer by inhibiting glucose-6-phosphate dehydrogenase (G6PD). Loss of Aldob promotes hepatocellular carcinogenesis (HCC), suggesting Aldob as a therapeutic target.

Area of Science:

  • Oncology
  • Metabolic pathways
  • Cancer biology

Background:

  • Metabolic reprogramming is crucial in cancer, but its role in hepatocellular carcinogenesis (HCC) is not fully understood.
  • Aldolase B (Aldob) function in HCC development requires further elucidation.

Purpose of the Study:

  • To investigate the role of hepatic aldolase B (Aldob) in hepatocellular carcinogenesis (HCC).
  • To identify the molecular mechanism by which Aldob influences HCC progression.
  • To explore potential therapeutic strategies targeting metabolic pathways in HCC.

Main Methods:

  • Analysis of Aldob and glucose-6-phosphate dehydrogenase (G6PD) levels in human HCC tumors.
  • Generation and analysis of Aldob knockout mouse models (global and liver-specific).
  • Pharmacological and genetic inhibition of G6PD in mouse models.
  • Biochemical assays to determine the interaction between Aldob, G6PD, and p53.

Main Results:

  • Decreased Aldob and increased G6PD expression in human HCC correlate with poor patient prognosis.
  • Aldob deficiency promotes HCC development in mice by enhancing G6PD activity and pentose phosphate pathway (PPP) metabolism.
  • G6PD inhibition suppresses HCC, while Aldob restoration attenuates tumorigenesis in knockout mice.
  • Aldob forms a complex with G6PD and p53, potentiating p53-mediated G6PD inhibition independently of Aldob's enzymatic activity.

Conclusions:

  • Loss of hepatic Aldob contributes to HCC through enhanced G6PD activity and PPP metabolism.
  • Aldob acts as a tumor suppressor in HCC by forming a complex that inhibits G6PD.
  • Targeting the Aldob-G6PD-p53 axis represents a potential therapeutic strategy for HCC.

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