Figure 4 | Scientific Reports

Figure 4

From: Knockdown of Malic Enzyme 2 Suppresses Lung Tumor Growth, Induces Differentiation and Impacts PI3K/AKT Signaling

Figure 4

Supplementation of exogenous cell-permeable DMM mimics the ME2 deficient phenotype.

(a), Depletion of ME2 in A549 cells cause malate accumulation analyzed by LC-MS. (b), Malate in ME2 knockdown and control cells were analyzed by malate assay kit. (c), Treatment of A549 control and ME2 knockdown cells with DMM inhibits cell proliferation. (d), ME2 knockdown cells showed more sensitive to exogenous DMM treatment. (e), Exogenous DMM treatment induces A549 control and ME2 knockdown cells undergoing necrosis. (f), Exogenous DMM treatment enhances ROS production. Top: A549 cells treated with 20 mM DMM and the ROS-induced by DMM were analyzed in different time as indicated; Bottom: ROS-induced by different concentrations of DMM as indicated were analyzed. (g), Exogenous of DMM treatment induces A549 lung cancer cells differentiation and AKT and PDK1 activity inhibition. The full-length blots are presented in Supplemental Figure S15. (h), Quantitatively analysis p-Akt in “g” by densitometry assay.

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