Fig. 1: PTEN loss induces cytoplasmic accumulation of ME2.
From: AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis
a, b Electron microscopic immunogold staining of ME2 in PTEN-normal expressing (A549, H1299, PC9, U2OS) and Pten-null (PC3 and U87) cells (a), as well as in HepG2 and PC9 cells expressing vector control shRNA or shRNA targeting PTEN (b) using an anti-ME2 antibody (CST, cat#35939). Arrows indicate ME2 staining. Black arrows represent mitochondrial localization of ME2, and red arrows represent cytosolic or non-mitochondrial localization of ME2. Dashed circles indicate mitochondria. Scale bars, 200 nm. c Structured Illumination super-resolution Microscope (SIM) imaging of ME2 in HepG2 cells stable expressing control shRNA or PTEN shRNA. White arrows represent mitochondrial localization of ME2, and green arrows represent cytosolic or non-mitochondrial localization of ME2. Scale bars, 10 μm. d Immunoblot analysis of ME2 expression in cytoplasmic fractions and whole-cell lysates of HepG2 cells stably expressing control shRNA or PTEN shRNA. β-tubulin and COXIV served as loading controls as well as cytosolic and mitochondrial markers, respectively. All data are representative of three independent experiments.
