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Knockdown of Malic Enzyme 2 Suppresses Lung Tumor Growth, Induces Differentiation and Impacts PI3K/AKT Signaling
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Knockdown of Malic Enzyme 2 Suppresses Lung Tumor Growth, Induces Differentiation and Impacts PI3K/AKT Signaling
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Journal Article
Knockdown of Malic Enzyme 2 Suppresses Lung Tumor Growth, Induces Differentiation and Impacts PI3K/AKT Signaling
2014
Overview
Mitochondrial malic enzyme 2 (ME2) catalyzes the oxidative decarboxylation of malate to yield CO
2
and pyruvate, with concomitant reduction of dinucleotide cofactor NAD
+
or NADP
+
. We find that ME2 is highly expressed in many solid tumors. In the A549 non-small cell lung cancer (NSCLC) cell line, ME2 depletion inhibits cell proliferation and induces cell death and differentiation, accompanied by increased reactive oxygen species (ROS) and NADP
+
/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 (DMM) mimics the ME2 knockdown phenotype. Both ME2 knockdown and DMM treatment reduce A549 cell growth
in vivo
. Collectively, our data suggest that ME2 is a potential target for cancer therapy.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
1-Phosphatidylinositol 3-kinase
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/ 13/106
/ 13/109
/ 13/2
/ 13/31
/ 13/51
/ 13/89
/ 13/95
/ 96/34
/ Adult
/ Aged
/ Animals
/ Cell Differentiation - drug effects
/ Cell Differentiation - genetics
/ Cell Proliferation - drug effects
/ Cell Proliferation - genetics
/ Child
/ Enzymes
/ Female
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Lung Neoplasms - drug therapy
/ Malate Dehydrogenase - genetics
/ Malate Dehydrogenase - metabolism
/ Male
/ NAD
/ NADP
/ Non-small cell lung carcinoma
/ Phosphatidylinositol 3-Kinases - metabolism
/ Proto-Oncogene Proteins c-akt - metabolism
/ Science
/ Signal Transduction - drug effects
/ Signal Transduction - genetics
/ Tensin
