Advances in molecular mechanism of gastric cancer peritoneal metastasis

Table 6 Key pathways and mechanisms in metabolic reprogramming in gastric cancer peritoneal metastasis

Metabolic pathway	Key molecule/enzyme	Mechanism of action	Functional	Clinical potential
Glycolysis (Warburg effect)	PKM2	Accelerated glucose metabolism; translocates to nucleus as co-activator	Promotes proliferation, invasion, metastasis	Target PKM2 (PKM2 inhibitors or PKM2 activators)
	LINC00589	Regulates alternative splicing of pyruvate kinase pre-mRNA toward PKM2 isoform	Drives Warburg effect	LINC00589 delivery via PMSNs
Lipid metabolism	FASN	Accelerated fatty acid anabolism	Promote proliferation, survival, and metastasis	FASN inhibitors
	PI3K-AKT-mTORC1	Upregulates monounsaturated fatty acid synthesis; inhibits phospholipid peroxidation	Confers ferroptosis resistance	mTORC1 inhibitor combined with ferroptosis inducer
	LINC00924/hnRNPC/Mnk2	Regulates alternative splicing of Mnk2 → inhibits p38 MAPK → activates PPARα	Enhances fatty acid oxidation and uptake	PPARα inhibitors
Amino acid metabolism	Glutamine	Converted to glutamate → enters TCA cycle; regulates redox status and signal transduction	Promotes proliferation, invasion, metastasis	Glutaminase inhibitors
Neural-tumor crosstalk	Mitochondrial transfer	Neurons donate functional mitochondria to tumor cells via intercellular transfer	Enhances oxidative phosphorylation; provides bioenergetic support for metastasis	Chemical denervation

This table summarizes the core metabolic pathways involved in gastric cancer peritoneal metastasis: Glycolysis, lipid metabolism, and amino acid metabolism. It highlights key enzymes, mechanisms of action, functional consequences, and therapeutic opportunities. PKM2: Pyruvate kinase M2; PMSNs: Polyethyleneimine-modified mesoporous silica nanoparticles; FASN: Fatty acid synthase; PI3K: Phosphatidylinositide 3-kinase; AKT: Protein kinase B; mTORC1: Mechanistic target of rapamycin complex 1; MAPK: Mitogen-activated protein kinase; PPARα: Peroxisome proliferator-activated receptor alpha; TCA: Tricarboxylic acid.