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Literature summary for 1.1.1.40 extracted from

  • Ren, J.G.; Seth, P.; Clish, C.B.; Lorkiewicz, P.K.; Higashi, R.M.; Lane, A.N.; Fan, T.W.; Sukhatme, V.P.
    Knockdown of malic enzyme 2 suppresses lung tumor growth, induces differentiation and impacts PI3K/AKT signaling (2014), Sci. Rep., 4, 5414.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine enzyme ME2 is a potential target for cancer therapy Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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-
-

Source Tissue

Source Tissue Comment Organism Textmining
A-549 cell
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Homo sapiens
-

Synonyms

Synonyms Comment Organism
malic enzyme 2
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Homo sapiens
ME2
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Homo sapiens

Expression

Organism Comment Expression
Homo sapiens supplementation by cell permeable exogenous dimethylmalate (DMM) in A-549 cells mimics the ME2 knockdown phenotype down

General Information

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