Application | Comment | Organism |
---|---|---|
medicine | enzyme ME2 is a potential target for cancer therapy | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
A-549 cell | - |
Homo sapiens | - |
Synonyms | Comment | Organism |
---|---|---|
malic enzyme 2 | - |
Homo sapiens |
ME2 | - |
Homo sapiens |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | supplementation by cell permeable exogenous dimethylmalate (DMM) in A-549 cells mimics the ME2 knockdown phenotype | down |
General Information | Comment | Organism |
---|---|---|
malfunction | knockdown of malic enzyme 2 suppresses lung tumor growth, induces differentiation and impacts PI3K/AKT signaling. In the A-549 non-small cell lung cancer cell line, ME2 depletion inhibits cell proliferation and induces cell death and differentiation, accompanied by increased reactive oxygen species (ROS) and NADP1/NADPH ratio, a drop in ATP, and increased sensitivity to cisplatin. ME2 knockdown impacts phosphoinositide-dependent protein kinase 1 (PDK1) and phosphatase and tensin homolog (PTEN) expression, leading to AKT inhibition. Depletion of ME2 leads to malate accumulation and pyruvate decrease, and exogenous cell permeable dimethyl-malate mimics the ME2 knockdown phenotype. Both ME2 knockdown and dimethyl-malate treatment reduce A-549 cell growth in vivo. Survival of ME2 knockdown cells is exquisitely dependent on glucose. Phenotype, overview | Homo sapiens |