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Table 1 Main oncogenic drivers and associated metabolic alterations in PLC

From: Metabolic reprogramming in the tumor microenvironment of liver cancer

Oncogenic drivers

Target molecules

Dysregulated metabolic pathways

PLC types (proportions)

References

MYC OE

GLUT1/2

Glycolysis

HCC (15%)

[82, 83, 85]

 

HK2

Serine biosynthesis

iCCA (6%)

 
 

PKL/PKM

   
 

PSPH

   

TP53 mut

GLUT1/4

Oxidative glycolysis

HCC (58%)

[86, 90]

   

iCCA (21%)

 

CTNNB1 mut

PPARα

FAO

HCC (19%)

[65]

 

GS

mTORC1

  

APOB mut

 

VLDL secretion

HCC (10%)

[77]

ALB mut

 

Albumin production

HCC (9%)

[78]

KRAS mut

GLUT1

Glycolysis

iCCA (17%)

[90]

IDH1/2 mut

αKG-dependent dioxygenases

TCA

iCCA (17%)

[92]

BAP1 mut

Histone H2A and mitochondrial ubiquitination

Gluconeogenesis and lipid homeostasis

iCCA (12%)

[79]

  1. OE overexpression; Mut mutation; GLUT glucose transporter; HK2 hexokinase 2; PKL/PKM pyruvate kinase isoforms L/M; PSPH phosphoserine phosphatase; PPARα peroxisome proliferator-activated receptor-α; GS glutamine synthetase; αKG α-ketoglutarate; FAO fatty acid oxidation; VLDL very low-density lipoprotein; and TCA tricarboxylic acid