Osteoactivin expression is required for the invasive phenotype of in vivo selected bone metastatic 4T1 breast cancer cells. Osteoactivin expression is.

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Epithelial-to-Mesenchymal Transitions Circulating Tumor Cells

Epithelial-to-Mesenchymal Transitions Circulating Tumor Cells

Volume 15, Issue 6, Pages (June 2009)

CDK2 is highly expressed in colon cancer cells and curcumin selectively suppresses HCT116 cell proliferation. CDK2 is highly expressed in colon cancer.

Pirh2 promotes p73 ubiquitination in vivo.

Decreased expression of cell cycle– and apoptosis-related genes in Aml1-excised leukemia cell. Decreased expression of cell cycle– and apoptosis-related.

Appearance of prominin-1-containing membrane particles in the culture medium upon differentiation of Caco-2 cells. Appearance of prominin-1-containing.

Highly related T9 and T3 sarcoma cells show distinct tumor growth patterns but similar PD-L1 expression kinetics in vivo. Highly related T9 and T3 sarcoma.

Knocking down Wnt3 increases the cells' response to trastuzumab and reduces cells' invasiveness. Knocking down Wnt3 increases the cells' response to trastuzumab.

JAK3A572V mutation causes constitutive JAK3 activity and IL-2–independent proliferation of NKTCL cells. JAK3A572V mutation causes constitutive JAK3 activity.

IL-6 inhibits insulin-induced formation of p85/IRS-1 complexes.

MYC degradation screen identifies a compound that stabilizes MYC protein. MYC degradation screen identifies a compound that stabilizes MYC protein. (A)

Induction of apoptosis by NMT siRNAs.

Oncogenic Ras signaling activates SFKs and promotes CDCP1-dependent invasion in 3-dimensional (3D) collagen raft culture of HCK. A, HCK1T-E cells, HCK1T-E.

VP16-E2 is a more potent transcriptional activator than Gal4-VP16.

Gramicidin A (GA) decreases HIF protein expression in RCC cells.

CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.

Induction of CDCP1 is regulated by Ras in NSCLC cells.

Silencing hOGG1 triggers caspase-3 and caspase-7 activation in response to H2O2 in GM00637 cells. Silencing hOGG1 triggers caspase-3 and caspase-7 activation.

The role of p53 in H2O2-mediated cell death of hOGG1-deficient H1299 lung carcinoma p53 null cells. The role of p53 in H2O2-mediated cell death of hOGG1-deficient.

In vitro invasion assays were done in the Chemicon invasion chamber containing extracellular matrix. In vitro invasion assays were done in the Chemicon.

TGF-β1 modulates extracellular matrix–mediated MT1-MMP expression.

PELP1 regulates the expression and activities of MMPs in ER-negative cells. PELP1 regulates the expression and activities of MMPs in ER-negative cells.

MAPJD expression in lung cancers.

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.

SiRNA silencing of CDH3, CLDN1, KRT23, and MMP7 (A–D) in adenoma and CRC cell lines significantly reduces cell proliferation. siRNA silencing of CDH3,

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.

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The expression of d-GM3 facilitates melanoma cell migration and invasion by activating p38 MAPK, not ERK. A, cell migration and invasion in d-GM3–positive.

Expression of CRC stem cell markers and L1 in CRC cells.

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.

SAF-1 expression in clinical breast cancer tissues.

HDACI treatment leads to down-regulation of AR and neuroendocrine transdifferentiation of LNCaP or LAPC4 cells. HDACI treatment leads to down-regulation.

In vivo tumorigenicity of MKN-1 cells with sustained suppression of HDAC2. In vivo tumorigenicity of MKN-1 cells with sustained suppression of HDAC2. A,

Microarray analysis of global gene expression profiles of PC-3 and derivative cell lines. Microarray analysis of global gene expression profiles of PC-3.

Consistency of conversion of GR to urinary ITC in 3 high converter phenotypes who were tested on 5 to 7 occasions (selected from the 131 determinations.

Combination of miR-520d-3p and EphA2 siRNA treatment shows enhanced EphA2 inhibition and antitumor efficiency in vitro. Combination of miR-520d-3p and.

Pirh2 represses p73-dependent transactivation.

Effects of HDAC2 inactivation on the invasive potential of human gastric cancer cells. Effects of HDAC2 inactivation on the invasive potential of human.

The effects of HDAC2 knockdown on cell-cycle proteins.

Platinum-based chemotherapy increased TXNIP expression, and overexpression of TXNIP enhanced the effectiveness of this therapy. Platinum-based chemotherapy.

Expression of versican promoted breast cancer cell tumor formation and self-renewal in vivo. Expression of versican promoted breast cancer cell tumor formation.

RUNX3 depletion induces cellular senescence and inflammatory cytokine expression in cells undergoing TGFβ-mediated EMT. A, Cells were transfected with.

HMQ1611 inhibited breast tumor growth in mice.

Osteoactivin is overexpressed in aggressively bone metastatic 4T1 subpopulations versus weakly bone metastatic breast cancer populations. Osteoactivin.

LRP1 is necessary for rK5-induced apoptosis of primary human brain MvEC. LRP1 is necessary for rK5-induced apoptosis of primary human brain MvEC. Irradiated.

Enhanced expression of Cap43 gene by nickel in breast cancer cell lines. Enhanced expression of Cap43 gene by nickel in breast cancer cell lines. Expression.

Tumorigenicity of GR CAFs

SAHA blocks IR-induced increase of RAD51 protein in MM cells.

HOXA11-AS acts as a ceRNA for miR-1297.

Decreased dopamine uptake following downregulation of SLC6A3.

The interaction of PALB2 with BRCA1 is required for the assembly of PALB2, BRCA2, and RAD51 nuclear foci. The interaction of PALB2 with BRCA1 is required.

A, left: LNCaP cells were cultured in media containing complete serum, treated for 24 hours with either ethanol control (0.01%), ABT888 (2.5 mmol/L), or.

Expression and induction of HER2 and HPSE in 231BMBC cells.

Treatment with a Ron inhibitor significantly reduces metastatic outgrowth. Treatment with a Ron inhibitor significantly reduces metastatic outgrowth. A,

Effect of MIF siRNA on the production of MMP-13 induced by LPA

Establishment of HeLa/rtTAA/TRE-N1-IC cell line.

P38 activation requires a d-GM3–dependent membrane molecular complex of uPAR, caveolin-1, and integrin α5β1. p38 activation requires a d-GM3–dependent.

Fig. 1 RNA methyltransferase METTL14 and demethylase ALKBH5 promote growth and invasion of breast cancer cells. RNA methyltransferase METTL14 and demethylase.

PLK1 is a crucial downstream effector of PDK1 for MYC activation and cell survival. PLK1 is a crucial downstream effector of PDK1 for MYC activation and.

A, indicated model systems were cultured in media containing complete serum, harvested, and lysed; total protein was separated by SDS-PAGE, transferred.

Effects of NMT siRNAs on MARCKS and c-Src.

KDM4A levels affect the distribution of translation initiation factors

Loss of NQO1 expression inhibits invasion of NSCLC

Knockdown of ROR1 increases the invasive potential of melanoma cells in vitro and in vivo. Knockdown of ROR1 increases the invasive potential of melanoma.

CREB1 binds at the proximal region of the TGFB2 promoter and induces its transcriptional activation. CREB1 binds at the proximal region of the TGFB2 promoter.

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.

D-GM3 promotes uPAR clustering on the cell surface and activates p38 MAPK. A, uPAR expression in cells was either knocked down by treatment with 4 independent.

Sp1 complementation assay.

Presentation transcript:

Osteoactivin expression is required for the invasive phenotype of in vivo selected bone metastatic 4T1 breast cancer cells. Osteoactivin expression is required for the invasive phenotype of in vivo selected bone metastatic 4T1 breast cancer cells. A. Seventy-two hours posttransfection, immunoblot analyses were done on control and osteoactivin (OA) siRNA–transfected 592 and 593 BM2 cells, using antibodies against osteoactivin (top), MMP-3 (middle), and α-tubulin (bottom; data not shown for 593 BM2 cells). B. Motility (top) and invasion (bottom) assays were done as described in Fig. 3. Significant differences in invasion were observed between 592 and 593 BM2 cells treated with osteoactivin siRNAs compared with 592 and 593 BM2 cells treated with control siRNAs (*, P < 0.01; **, P < 0.03). Results are derived from at least three independent experiments. C. Representative images are shown for both motility (top) and invasion (bottom). D. Quantitative real-time PCR analysis was done to examine MMP-3 expression in the in vivo selected bone metastatic populations compared with parental 4T1 cells. MMP-3 expression was first normalized to GAPDH levels and expressed as the fold change over 4T1 parental cells. April A.N. Rose et al. Mol Cancer Res 2007;5:1001-1014 ©2007 by American Association for Cancer Research