ST6GalNAc2 expression enhances tumor cells interaction with the vasculature. ST6GalNAc2 expression enhances tumor cells interaction with the vasculature.

Slides:



Advertisements
Similar presentations
Camacho et al, Fig. S1 a c e b d f
Advertisements

Figure S1. qPCR analysis of the EMT markers ZEB2 and SNAI1 in Syndecan-1 and control siRNA transfected MDA-MB-231 and MCF-7 cells reveals no significant.
AF647-RIS is internalized by TAMs in vivo.
by Satoshi Kokura, Robert E. Wolf, Toshikazu Yoshikawa, D
CDK4 is required for the hormone-independent growth of ER+ breast cancer cells. CDK4 is required for the hormone-independent growth of ER+ breast cancer.
NETosis is regulated by ECM molecules and promotes CD5+ B–cell proliferation through NF-κB activation. NETosis is regulated by ECM molecules and promotes.
Figure S1A. Supplementary Figure S1A. In vitro infectivity of vaccinia virus after exposure to cavitation. A dose of 1x106 vaccinia virus was mixed with.
Attenuated MDSC-suppressive activity and metastasis development in IDO-deficient mice is rescued by IL-6. Attenuated MDSC-suppressive activity and metastasis.
BV6 increases tumor burden in bone.
Validation of St6GalNAc2 as a metastasis suppressor gene.
Suppressive effect of CD39+CD73+ melanoma cells on T-cell proliferation, and reversion of this effect via treatment with the CD39-blocking antibody, CD39.
Fig. 3. Wisper controls CF behavior and survival.
MEKi reduces sheddase activity via increased TIMP1 association, and TIMP1 neutralization enhances MAPKi efficacy. MEKi reduces sheddase activity via increased.
Functional interaction of Eμ-Tcl1 tumor cells with FDC networks.
nab-Paclitaxel promotes elevated intratumoral gemcitabine levels.
Microarray analysis of phospho-Twist1–responsive genes.
A C D B Asynchronous nM Nocodazole 150 ► 100 ► 75 ►
Fig. 5. pKL cells abrogate the autoimmune response in vitro.
A role for galectin-3 in promoting lung colonization in ST6GalNAc2-silenced cells. A role for galectin-3 in promoting lung colonization in ST6GalNAc2-silenced.
Fig. 5 Local gel scaffold for T cell memory response.
DC-derived EV differentiate monocytes.
The selective PI3K inhibitor A66 suppresses PIP3 accumulation, AKT phosphorylation at Thr308, and YAP/TAZ–regulated gene expression in PDAC cells. The.
Fig. 2. CD31 provides robust NP targeting in vitro but slow kinetics.
Role of HER2 in mediating acquired resistance to EGFR inhibition.
Fig. 5 DMN-Tre labeling is selective for live mycobacteria.
Nox1 as a potential therapeutic target to inhibit matricellular-mediated endothelial senescence. Nox1 as a potential therapeutic target to inhibit matricellular-mediated.
TriKE–treated NK cells overcome MDSC-induced immune suppression.
Fig. 5. Prip silencing enhances the co-localization of GABARAP with insulin vesicles and β-tubulin.Co-localization of GABARAP (green) with insulin (red)
Mammary cell proliferation is inhibited when LAD1 is depleted.
Fig. 4 Labeling of Msmeg with DMN-Tre is fast and specific and depends on Ag85A function. Labeling of Msmeg with DMN-Tre is fast and specific and depends.
Arginine-to-lysine mutations conferring TRIM22 restriction and lysine-to-arginine mutations causing loss of TRIM22 restriction. Arginine-to-lysine mutations.
(A) Relative expression levels of the top most down-regulated genes in LATS2L breast tumors (TCGA-BRCA dataset, see Fig 1) in the panel of breast cancer.
Exosome-mediated inhibition of T cells is reversible.
Dynamics of actin-binding proteins in the ICAM-1 complex.
CD151-knockdown cells show an aberrant spreading response to PMA
BCX inhibits lamellipodia formation in lung cells.
Adaptive NK cells resist immunosuppression in the tumor microenvironment. Adaptive NK cells resist immunosuppression in the tumor microenvironment. FACS-sorted.
Fig. 4 Cdc42 enhances the cellular uptake of EVs.
GC reaction is impaired in NOTCH2 knock-in mice.
Tumor MMP-1 functionally regulates the permeability of endothelial cell barriers and contributes to HEp3-hi/diss transendothelial migration. Tumor MMP-1.
CCG regulates cellular localization and blocks target gene expression of MRTF. A, SK-Mel-147 cells were cotransfected with RhoC and the SRE.L reporter.
Spn promotes Rac1 GTPase activation in glioblastoma (GBM) cells.
Overexpression of DDB2 reduces invasive abilities in lungs of aggressive breast tumor cells. Overexpression of DDB2 reduces invasive abilities in lungs.
ARID1A promotes DSB end resection.
Tumor cell clusters arise from cellular aggregation.
RUNX3 depletion induces cellular senescence and inflammatory cytokine expression in cells undergoing TGFβ-mediated EMT. A, Cells were transfected with.
Deletion of Tgfbr2 in myeloid cells elevated IFN-γ production in CD8+ T cells, and systemic IFN-γ neutralization diminished metastasis inhibition in Tgfbr2MyeKO.
CD44 depletion blocks tumor cell aggregation and lung metastasis in vivo. CD44 depletion blocks tumor cell aggregation and lung metastasis in vivo. A,
Trametinib and combination promote moDC maturation and decrease moDC viability. Trametinib and combination promote moDC maturation and decrease moDC viability.
CCR5 enhances both HDR and SSA DNA repair.
Adhesion of T-cell clones to autologous tumor cells under shear stress
Dgk inhibitors enhance the cytotoxic capacity of impaired human mesoCAR-transduced T cells. Dgk inhibitors enhance the cytotoxic capacity of impaired human.
Snail-induced multinucleation follows midbody persistence.
PTEN-deficient prostate cancer cells exhibit constitutive macropinocytosis. PTEN-deficient prostate cancer cells exhibit constitutive macropinocytosis.
Apoptotic cell debris induces AXL-dependent cell migration.
Blocking αvβ3/galectin-3 binding with GCS-100 selectively kills KRAS-addicted lung cancer cells. Blocking αvβ3/galectin-3 binding with GCS-100 selectively.
NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro. NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro.
Increased tumorigenic activities of TIM-3–expressing RCC cells.
KRAS-addicted lung cancer cells need αvβ3/galectin-3 to maintain low ROS levels. KRAS-addicted lung cancer cells need αvβ3/galectin-3 to maintain low ROS.
Tumor spheroid induces mesothelial cell migration.
Interaction of cancer spheroids with mesothelium prompts mesothelial cell clearance. Interaction of cancer spheroids with mesothelium prompts mesothelial.
Moderate-affinity vaccine antigens elicited greatest antitumor response. Moderate-affinity vaccine antigens elicited greatest antitumor response. Wild-type.
The effect of βAR signaling on the generation of a cytotoxic CD8+ T-cell response in vivo. The effect of βAR signaling on the generation of a cytotoxic.
In vivo shRNA screening strategy.
Dose-dependent effect of IP6 feeding on angiogenesis in prostate of TRAMP mice. Dose-dependent effect of IP6 feeding on angiogenesis in prostate of TRAMP.
CD38 regulates tumor growth and metastasis by adenosine-mediated CD8+ T-cell suppression. CD38 regulates tumor growth and metastasis by adenosine-mediated.
Bezafibrate increases the number of effector CTLs by enhancing their survival capacity and proliferation. Bezafibrate increases the number of effector.
Combining IGF1R inhibitors with MEK or RAF inhibitors enhances the differential impact upon mutant KRAS cells. Combining IGF1R inhibitors with MEK or RAF.
SCLC in CMV TKO mice arises from an alternative cell of origin.
Varying the MHC-I affinity, TCR affinity or antigen dose alters the phenotype of CD8 T cells ex vivo. Varying the MHC-I affinity, TCR affinity or antigen.
Presentation transcript:

ST6GalNAc2 expression enhances tumor cells interaction with the vasculature. ST6GalNAc2 expression enhances tumor cells interaction with the vasculature. A, model of tumor:endothelial interactions modulated by ST6GalNAc2 expression levels. See text for details. B, shST6 and shNTC ZR75.1 cells (see Supplementary Fig. S5A for qPCR analysis) were labeled with CellTracker dyes, mixed at a 1:1 ratio, and co-perfused over activated HUVECs under flow conditions (see Methods) in the absence (left and Supplementary Movie S1) and presence (right and Supplementary Movie S2) of the galectin-3 inhibitor GCS-100. Data shown are the mean number of shNTC and shST6 cells that adhered to HUVECs at 1, 5, and 10 minutes. Equivalent results were obtained in three independent experiments. Two-way ANOVA with Bonferroni posttest was used to generate P values. *, P < 0.05; **, P < 0.01. C and D, 4 × 104 4T1-Luc cells transfected with siNTC or siST6 in the presence or absence of siGAL3 were added to monolayers of HUVEC or sEND endothelial cells in 24-well plates in the presence or absence of 100 mmol/L lactose and incubated for 30 minutes at 37°C. Wells were washed and adherent cells quantified. Data shown are mean values from triplicate samples ±SEM. Student t test was used to generate P values. Equivalent results were obtained in three or two independent experiments, respectively. E and F, aggregation of tumor cells transfected with siNTC or siST6, with or without siGAL3 cotransfection, in the lung was quantified for the mice shown in Fig. 5D (4T1-Luc cells) and Fig. 5G (MDA-MB-453 cells) at 24 and 5 hours, respectively. Data shown are mean size of tumor cell aggregates/fov for the 4 mice in each group ±SEM. Student t test was used to generate P values. Representative confocal images are shown. Scale bar, 100 μm. ns, not significant; AU, arbitrary unit. Nirupa Murugaesu et al. Cancer Discovery 2014;4:304-317 ©2014 by American Association for Cancer Research