Table 2.
Metabolic reprogramming drugs in GC.
Agent | Type of metabolic reprogramming | Target pathway and protein | Observation | |
---|---|---|---|---|
Molecular targeted drugs | MK2206 | Glycolysis | PI3K/Akt | Reversion the trastuzumab resistance (139) |
Rhodium (III) complex 6 | TCA cycle, glycolysis, and AA pathways | STAT3 | Reversion the trastuzumab resistance (141) | |
Apatinib | Glycolysis | VEGFR2/AKT1/SOX5/GLUT4 | Inhibition the viability and proliferation (145) | |
2-deoxy glucose | Glycolysis | JNK (168) | Inhibition the angiogenesis (147) | |
PA-1, PA-2 | Glycolysis | PFKFB3 | Inhibition the angiogenesis (149) | |
Immunotherapy | Diclofenac | Glycolysis | MCT1, MCT4 | Improvement of the anti-PD1-induced T cell killing (156) |
6-diazo-5-oxo-l-norleucine | Glycolysis | Glutamine-utilizing enzymes | Increasing infiltration of CD8+ T cells and sensitized tumors to anti-PD1 therapy (157) | |
AZD1480, LY294002, rapamycin | Glycolysis | JAK2, PI3K, mTOR | Arresting the G0/G1, promoting the T-cell proliferation, reducing the PD-L1 (158) | |
Metformin | Glycolysis | mTOR/AKT (169) | Decreasing expression CTLA-4 of Treg cell (160) | |
Telaglenastat | Glutamine | Glutamine enzymes | Increasing effector T cells (161) | |
Natural compounds | Salazosulfapyridine | Glycolysis | Cystine/glutamate | Increasing ROS, inhibition cell proliferation (164) |
Crocin | Mitochondrial Dysfunction (170). | HIF-1α | Inhibition the EMT, migration, invasion in GC (165) |
TCA, tricarboxylic acid; AA, amino acid.