Treatment with LY294002 for 4 days inhibits PI3K phosphorylation activity and decreases GPx activity.

<p>The effect of 20 μM LY294002 treatment of KU812a cells on GPx activity levels alone or in combination with 150 nM imatinib is shown. Data presented is derived from three independent experiments. * =  <i>P</i><0.001, ** = <i>P</i><0.01.</p

Quantitative identification and bioinformatics analysis of tumor tissue proteins assayed by iTRAQ.

<p><b>(A)</b> All 132 differentially accumulated proteins were classified into three groups: biological process, molecular function, and cellular component through GO analysis. <b>(B)</b> The numbers of lipid/glucose metabolism-related proteins were shown through GO analysis.</p

GPx-1 protein and activity levels are decreased by exogenous Bcr-Abl in MDA-MB-231.

<p>MDA-MB-231 cells transfected with a GFP-tagged Bcr-Abl vector and the transfection success was as assessed by fluorescence microscopy (A). The effect of ectopic Bcr-Abl expression on GPx enzyme activity in MDA-MB-231 cells. GPx activity was decreased 0.6-fold by ectopic expression of Bcr-Abl. Data shown is representative of one experiment. Two independent experiments were performed. * = <i>P</i><0.001. Error bars indicate S.D.</p

Hypothetic pathways of SBP1-mediated anti-cancer functions <i>in vivo</i>.

<p>SBP1-mediated anti-cancer effects may be through lipid/glucose metabolism. The possible functional regulation between SBP1 and related proteins is illustrated.</p

Identified differentially accumulated proteins related to lipid metabolism.

<p>Identified differentially accumulated proteins related to lipid metabolism.</p

Rapamycin increases levels of GPx-4, MnSOD and pS6 protein levels in cell lines.

<p>The effect of 1 ng/mL rapamycin on GPx-4 and MnSOD and pS6 protein levels in KU812a, MEG-01, GM10832 and MDA-MB-231 is shown. GPx-4 by 3-day 1 ng/mL rapamycin treatment in KU812a and MEG-01 (<i>P</i> > 0.2), but was increased 3-fold in GM10832 (<i>P</i> = 0.05) and 6-fold in MDA-MB-231 cells (<i>P</i> = 0.02). The disappearance of pS6 signal following rapamycin treatment indicates inhibition of mTOR. Data shown is representative of three independent experiments.</p

Quantitative identification and bioinformatics analysis of tumor tissue proteins assayed by iTRAQ.

<p><b>(A)</b> All 132 differentially accumulated proteins were classified into three groups: biological process, molecular function, and cellular component through GO analysis. <b>(B)</b> The numbers of lipid/glucose metabolism-related proteins were shown through GO analysis.</p

The translational efficiency of UGA readthrough by the GPx-1 SECIS is not enhanced by rapamycin.

<p>Diagrammatic representation of the pLNCX-UGA-GPx-1 reporter construct used for quantification of UGA read-through, containing the GPx-1 SECIS element (A). The effect of rapamycin (1 ng/mL), selenium (100 nM), or both on the translational efficiency of UGA readthrough in MDA-MB-231 cells infected with the pLNCX-UGA-GPx1 SECIS reporter construct as assessed by determining luciferase activity; relative luciferase levels were normalized to β-galactosidase levels to calculate translational efficiency (B). SECIS-dependent translational efficiency was not increased following 1 ng/mL rapamycin treatment, but was increased 2.6-fold by incubation of cells containing the reporter construct with selenium. Data shown represents two independent experiments. * = <i>P</i><0.001. Error bars indicate the S.D. The effect of rapamycin on U49C GPx-1 levels was determined by immunoblotting for GPx-1 by western blot analysis (C).</p

Rapamycin enhances GPx-1 protein and enzyme activity levels in all cell lines investigated.

<p>The effect of rapamycin on GPx-1 activity (A) and protein levels (B) in KU812a, MEG-01 GM10832 or MDA-MB-231 is shown. The effect of rapamycin on steady-state GPx-1 transcript levels as determined by RT-qPCR and normalization of GPx-1 Ct values to Ct values for 18s RNA (C). Rapamycin significantly increased protein respectively 3-fold and 1.3-fold in KU812a and MEG-01 (<i>P</i> = 0.05). Steady state transcript levels for GPx-1 were unaffected by treatment with rapamycin in KU812a. Data shown is representative of three independent experiments. * = <i>P</i><0.001, ** = <i>P</i><0.01. † = <i>P</i><0.05. Error bars indicate S.D.</p

GPx-1 levels are enhanced in a dose- and time-dependent manner following imatinib treatment.

<p>The dose- and time-dependent increases in GPx activity following 100 nM and 150 nM imatinib treatment of KU812a cells for 7 days (A) or 150 nM imatinib treatment for 3 or 7 days (B). The effect of imatinib treatment on GPx1 protein levels. Data shown is representative of thee independent experiments were performed (C). * = <i>P</i><0.001, † = <i>P</i><0.05, compared to 100 nM or 3-day imatinib treatment. Error bars indicate S.D.</p