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  • Image homogeneity Contrast Location image variations


    Image homogeneity Contrast Location image variations Correlation Image linearity Entropy Randomness of the gray levels Sum of squares (variance) Spread in the gray-level distribution Difference entropy Randomness of the difference of neighboring voxels' gray levels Difference variance Variations of difference of gray levels between voxel pairs Inverse difference moment Image homogeneity Sum average Overall brightness Sum entropy Randomness of the sum of gray levels of neighboring voxels Sum variance Spread in the sum of the gray levels of voxel-pair distribution Information measure of correlation 1 Nonlinear gray-level dependence Information measure of correlation 2 Nonlinear gray-level dependence Maximum correlation coefficient Nonlinear gray-level dependence Kinetic curve assessment
    Maximum enhancement Maximum FLAG tag Peptide enhancement Time to peak (s) Time at which the maximum enhancement occurs Uptake rate (1/s) Uptake speed of the contrast enhancement Washout rate (1/s) Washout speed of the contrast enhancement Curve-shape index Difference between late and early enhancements Enhancement at first postcontrast time point Enhancement at first postcontrast time point Signal-to-enhancement ratio Ratio of the initial enhancement to the overall enhancement Volume of most enhancing voxels (mm3) Volume of the most enhancing voxels Total rate variation (1/s2) How rapidly the contrast will enter and exit from the lesion Normalized total rate variation (1/s2) How rapidly the contrast will enter and exit from the lesion Enhancement-variance kinetics
    Maximum variance of enhancement Maximum spatial variance of contrast enhancement over time Time to peak at maximum variance (s) Time at which the maximum variance occurs Enhancement-variance increasing rate (1/s) Rate of increase of the enhancement variance during uptake Enhancement-variance decreasing rate (1/s) Rate of decrease of the enhancement variance during washout
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    BBA - Molecular Cell Research
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    Adducins inhibit lung cancer cell migration through mechanisms involving T regulation of cell-matrix adhesion and cadherin-11 expression
    Susana Lechugaa,b, Parth H. Aminb, Aaron R. Wolenb, Andrei I. Ivanova,b,
    a Department of Inflammation and Immunity, Lerner Research Institute of Cleveland Clinic Foundation, Cleveland, OH 44195, United States of America
    b Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA 23298, United States of America
    Membrane skeleton
    Focal adhesions
    Actin cytoskeleton 
    Cell migration is a critical mechanism controlling tissue morphogenesis, epithelial wound healing and tumor metastasis. Migrating cells depend on orchestrated remodeling of the plasma membrane and the underlying actin cytoskeleton, which is regulated by the spectrin-adducin-based membrane skeleton. Expression of adducins is altered during tumorigenesis, however, their involvement in metastatic dissemination of tumor cells remains poorly characterized. This study investigated the roles of α-adducin (ADD1) and γ-adducin (ADD3) in regulating migration and invasion of non-small cell lung cancer (NSCLC) cells. ADD1 was mislocalized, FLAG tag Peptide whereas ADD3 was markedly downregulated in NSCLC cells with the invasive mesenchymal phenotype. CRISPR/Cas9-mediated knockout of ADD1 and ADD3 in epithelial-type NSCLC and normal bronchial epithelial cells promoted their Boyden chamber migration and Matrigel invasion. Furthermore, overexpression of ADD1, but not ADD3, in mesenchymal-type NSCLC cells decreased cell migration and invasion. ADD1-overexpressing NSCLC cells de-monstrated increased adhesion to the extracellular matrix (ECM), accompanied by enhanced assembly of focal adhesions and hyperphosphorylation of Src and paxillin. The increased adhesiveness and decreased motility of ADD1-overexpressing cells were reversed by siRNA-mediated knockdown of Src. By contrast, the accelerated migration of ADD1 and ADD3-depleted NSCLC cells was ECM adhesion-independent and was driven by the upregulated expression of pro-motile cadherin-11. Overall, our findings reveal a novel function of adducins as negative regulators of NSCLC cell migration and invasion, which could be essential for limiting lung cancer progression and metastasis.
    1. Introduction
    Cell migration is a critical mechanism that mediates plasticity of epithelial layers under normal conditions and in the disease state. For example, in the developing embryo and self-rejuvenating adult tissues, the coordinated migration of cells of different lineages plays key roles in the cell patterning, establishment of tissue boundaries and organ mor-phogenesis [1,2]. Furthermore, cell migration is essential for repairing epithelial layers damaged by environmental and inflammatory factors [3,4]. However, a dark side of epithelial cell motility is well recognized during tumorigenesis, where accelerated migration of cancer cells drives tumor dissemination and metastasis [5,6].