CLIC1 is upregulated in invadopodia of fibrin-embedded tumor and endothelial cells. CLIC1 is upregulated in invadopodia of fibrin-embedded tumor and endothelial.

Slides:



Advertisements
Similar presentations
Recruitment of VAMP3 to the phagocytic cup F-actin (red) and nuclei (blue) were stained in macrophages expressing GFP-VAMP3 (green) before confocal imaging.
Advertisements

Figure S1 a b c d DAPI Lgr β-catenin Merge
PD-1 and LAG-3 expression in MSI and MSS colorectal cancer specimens.
TIE2hi/VEGFAhi TEMs are present in the TMEM
Geographic distribution in situ of MSI and MSS colorectal cancer–infiltrating lymphocytes. Geographic distribution in situ of MSI and MSS colorectal cancer–infiltrating.
UUKV NSs interacts with MAVS
Confocal images of negative controls for Aβ42, Synaptophysin (syp), and PSD95 in hippocampal neurons. Confocal images of negative controls for Aβ42, Synaptophysin.
Immunofluorescence staining of virus-infected human placental explants
Fig. 2 In vitro assessment of hESC-RPE cell sheets.
IL32 prompts cell activation and cancer-related pathways.
PD-1 expression on HCC-infiltrating B cells and its clinical significance. PD-1 expression on HCC-infiltrating B cells and its clinical significance. A–H,
Confocal fluorescence microscopical images of 3-nitrotyrosine-positive blood vessels from a patient with mitochondrial disease. Confocal fluorescence microscopical.
Marker identification and quantification by StrataQuest, and confocal analysis of EV-containing tissue sections. Marker identification and quantification.
Subcellular localization of UUKV, HRTV, and SFTSV NSs
A1 A2 A3 A4 Figure S1. (A2, C2) hPDLSCs at P2 show low expression of p16 and p21 (red fluorescent) as indicated by double immunostaining. (A3, C3) Cells.
Inhibition of VEGFA or macrophage-specific ablation of Vegfa from TIE2hi/VEGFAhi TMEM macrophages reduces vascular permeability and tumor cell intravasation.
Distinct collagen structures in the upper and lower neonatal dermis (related to Fig 1)‏ Distinct collagen structures in the upper and lower neonatal dermis.
mpJX-594 effects on tumor burden and leukocyte influx.
ILK knockdown decreases mTOR signaling in PKD kidneys.
Imaging intracellular endosymbiont E. coli by fluorescent microscopy.
Fig. 1. Representative images of the four cell lines using fluorescence microscopy. Representative images of the four cell lines using fluorescence microscopy.
Fig. 1. Ovarian cancer spheroids can bud from a monolayer
High-affinity binding to the hypervariable region of the β1 I-like domain controls signaling to fibronectin fibrillogenesis. High-affinity binding to the.
SIRT1 is downregulated in human gastric cancer (GC).
High-affinity mutants of β3 integrin fail to stimulate RhoA activity and fibronectin fibrillogenesis. High-affinity mutants of β3 integrin fail to stimulate.
Effect of M-cadherin RNAi and GSK-3β inhibition on myogenic differentiation of C2C12 myoblasts. Effect of M-cadherin RNAi and GSK-3β inhibition on myogenic.
Fgfr3;4 mutant lungs display an increase in Mfap5, Igf1 and Fbn2 expression. Fgfr3;4 mutant lungs display an increase in Mfap5,Igf1and Fbn2 expression.
hADAR1 and hADAR2 co-localize within the nucleolus.
Fig. 1. Rnd2 and Rnd3 induce stress fibres whereas Rnd1 reduces stress fibres in endothelial cells.(A) Rnd mRNAs are expressed in HUVECs. Total RNA was.
Fibril-induced NM prions do not evolve from SGs.
Effect of M-cadherin RNAi on apoptosis in confluent C2C12 myoblasts.
Adipocytes sequester daunorubicin (DNR).
CLIC1 promotes tumor cell spreading through effects on MLCK
CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.
Interaction of aggregates with CAF network structures.
Peripheral CAF model. Peripheral CAF model. A, bright field (top) and fluorescence (bottom) micrographs of aggregates that contain RFP-tagged 344SQ cells.
CDCP1 colocalizes and interacts with MT1-MMP.
A, GP and GR epithelial tumor cells are equally responsive to gefitinib. A, GP and GR epithelial tumor cells are equally responsive to gefitinib. Equal.
Geldanamycin-induced endocytosis and down-regulation of ErbB2 in cells expressing ErbB2 only. Geldanamycin-induced endocytosis and down-regulation of ErbB2.
AXL is not expressed in human prostate tumors.
In vivo thrombosis of tumor vasculature.
A His/Pro-rich fragment of HRG is present in human tissue.
Spn promotes Rac1 GTPase activation in glioblastoma (GBM) cells.
CXCR4 expression levels of MDA-MB-231 cells at 48 hours posttransfection of CXCR4 siRNAs. CXCR4 expression levels of MDA-MB-231 cells at 48 hours posttransfection.
Anti-Flk-1 mAb treatment reduces vessel density in tumors.
EMT gene expression patterns of M-Wnt and E-Wnt cells in vitro and in vivo. EMT gene expression patterns of M-Wnt and E-Wnt cells in vitro and in vivo.
PVHA increased anti-PD-L1–mediated growth inhibition in 4T1/HAS3 tumors. PVHA increased anti-PD-L1–mediated growth inhibition in 4T1/HAS3 tumors. A, 4T1/HAS3.
Functional assessment of NF-κB activation in SKBR3 cells.
KPT-9274 shows specificity for attenuation of PAK4 targets preferentially in RCC cells. KPT-9274 shows specificity for attenuation of PAK4 targets preferentially.
Binding and antiproliferative effects of ANG4043 and anti-HER2 mAbs on tumor cells. Binding and antiproliferative effects of ANG4043 and anti-HER2 mAbs.
A macrophage-tumor cell cross-talk within Amppos tumors.
CLIC1 supports invadopodia formation in vitro and metastasis in vivo.
HMQ1611 inhibited breast tumor growth in mice.
Β-catenin knockout inhibits synovial sarcoma (SS) tumor growth in SYT–SSX2 transgenic mice. β-catenin knockout inhibits synovial sarcoma (SS) tumor growth.
TAMs directly contribute to tumor hypoxia.
GATA-3 immunostaining was scored semiquantitatively; tumors with
Purified Vpr induces double-strand breaks in vitro.
Fig. 5 C9orf72 knockdown disrupts autophagy induction.
The CCR5+ population of SUM-159 cells is enriched with tumor-initiating cells. The CCR5+ population of SUM-159 cells is enriched with tumor-initiating.
IFN treatment of human midgestation villous explants induces syncytial knot formation. IFN treatment of human midgestation villous explants induces syncytial.
Snail-induced multinucleation follows midbody persistence.
P53-expressing tumor cells circumvent mitosis, express markers consistent with a G1-like state, and become senescent in response to continuous chemotherapeutic.
Double knockdown of HER2/EGFR abolishes HPSE nucleolar localization in 231BR3 cells. Double knockdown of HER2/EGFR abolishes HPSE nucleolar localization.
Empty basement membrane sleeves and endothelial sprouts.
Influence of minocycline on TGF-β1 expression and TGF-β1–induced NF-кB activation in ovarian cancer cells. Influence of minocycline on TGF-β1 expression.
Identification of the molecular regulators of FLP formation.
EGF induces HPSE nucleolar localization in human BMBC cells.
SCLC initiated from pulmonary neuroendocrine cells metastasizes without upregulating NFIB. A and B, Mouse models of SCLC. Rb1flox/flox;Trp53flox/flox;p130flox/flox;R26mTmG.
Greater influx of PMNs and ST using PEGPH20/shIDO-ST.
The neuropod cells. The neuropod cells. (Top left) Neuropod cells synapse with sensory neurons in the small intestine, as shown in a confocal microscopy.
Presentation transcript:

CLIC1 is upregulated in invadopodia of fibrin-embedded tumor and endothelial cells. CLIC1 is upregulated in invadopodia of fibrin-embedded tumor and endothelial cells. A, confocal microscopy images of HUVEC or 786-0 cells embedded in fibrin clots for 1 or 2 hours after immunostaining with anti-CLIC1 (red). Nuclei are stained with draq5 (blue). B, confocal microscopy images of 24-hour fibrin-embedded HUVEC and 786-0 cells after immunostaining for β3 integrin (green) and CLIC1 (red). Nuclei are stained with draq5 (blue). C, fibrin-embedded 786-0 cells transformed with scrambled (shSCR, top) or β3 shRNA (shβ3, bottom) were fixed after indicated times and probed for CLIC1 (green) and F-actin (red). Nuclei are stained with draq5 (blue). Scale bars, 10 μm. Lisa A. Gurski et al. Mol Cancer Res 2015;13:273-280 ©2015 by American Association for Cancer Research