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Human Breast Carcinoma Cells (human + breast_carcinoma_cell)

Distribution by Scientific Domains
Medical Sciences50%
Life Sciences50%

Terms modified by Human Breast Carcinoma Cells

  • human breast carcinoma cell line
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    Selected Abstracts

    Membrane type-1 matrix metalloproteinase stimulates tumour cell-induced platelet aggregation: role of receptor glycoproteins

    BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2004
    David Alonso-Escolano
    Matrix metalloproteinase-2 (MMP-2) plays a role in agonist- and tumour cell-induced platelet aggregation (TCIPA). MMP-2 is synthesized as a proenzyme and is activated at the cell surface by membrane type-1 matrix metalloproteinase (MT1-MMP, MMP-14). The significance of tumour cell-associated MT1-MMP for TCIPA was investigated using human breast carcinoma MCF7 cells stably coexpressing the integrin ,v,3 with MT1-MMP, cells expressing ,v,3 alone and mock-transfected cells. Western blot and zymography confirmed that ,v,3/MT1-MMP cells expressed MT1-MMP and efficiently processed proMMP-2 to MMP-2. Aggregometry, phase-contrast and transmission electron microscopy and flow cytometry were used to characterize TCIPA induced by MCF7 cell lines. The aggregating potency of cells was: ,v,3/MT1-MMP >,v,3=mock cells, as shown by aggregometry and phase-contrast microscopy. Electron microscopy revealed close, membrane,membrane interactions between activated platelets and ,v,3/MT1-MMP cells during TCIPA. Inhibition of MMP-2 with the neutralizing anti-MMP-2 antibody (5 ,g ml,1) and o -phenanthroline (100 ,M) reduced aggregation induced by ,v,3/MT1-MMP cells. TCIPA induced by ,v,3/MT1-MMP cells was also reduced by inhibiting the generation and actions of ADP with apyrase (250 ,g ml,1) and 2-methylthio-AMP (2-MeSAMP) (30 ,M), but not N6 -methyl-2,-deoxyadenosine-3,,5,-bisphosphate (MRS2179) (30 ,M). Flow cytometry demonstrated that TCIPA enhanced expression of glycoprotein (GP) Ib and IIb/IIIa receptors not only on platelets but also on breast cancer cells. Thus, (a) human breast carcinoma cell surface-associated MT1-MMP, via activating proMMP-2, stimulates TCIPA; (b) ADP amplifies the effects of MMPs via stimulation of P2Y12 receptors and (c) both tumour- and platelet-derived GPIb and GPIIb/IIIa are involved in the aggregatory effects of MT1-MMP. British Journal of Pharmacology (2004) 141, 241,252. doi:10.1038/sj.bjp.0705606 [source]

    ,3-Tubulin is induced by estradiol in human breast carcinoma cells through an estrogen-receptor dependent pathway

    CYTOSKELETON, Issue 7 2009
    Jennifer Saussede-Aim
    Abstract Microtubules are involved in a variety of essential cell functions. Their role during mitosis has made them a target for anti-cancer drugs. However development of resistance has limited their use. It has been established that enhanced ,3-tubulin expression is correlated with reduced response to antimicrotubule agent-based chemotherapy or worse outcome in a variety of tumor settings. However little is known regarding the regulation of ,3-tubulin expression. We investigated the regulatory mechanisms of expression of ,3-tubulin in the MCF-7 cell line, a model of hormone-dependent breast cancer. Exposure of MCF-7 cells to estradiol was found to induce ,3-tubulin mRNA as well as ,3-tubulin protein expression. Conversely, we did not observe induction of ,3-tubulin mRNA by estradiol in MDA-MB-231 cells which are negative for the estrogen receptor (ER). In order to determine whether ,3-tubulin up-regulation is mediated through the ER pathway, MCF-7 cells were exposed to two ER modulators. Exposure to tamoxifen, a selective estrogen receptor modulator, completely abolished the ,3-tubulin mRNA induction due to estradiol in MCF-7 cells. This result was confirmed with fulvestrant, a pure antagonist of ER. These results demonstrate that the effect of estradiol on ,3-tubulin transcription is mediated through an ER dependent pathway. Cell Motil. Cytoskeleton 66:378,388, 2009. © 2009 Wiley-Liss, Inc. [source]

    CNTO 859, a humanized anti-tissue factor monoclonal antibody, is a potent inhibitor of breast cancer metastasis and tumor growth in xenograft models

    INTERNATIONAL JOURNAL OF CANCER, Issue 6 2007
    Cam V. Ngo
    Abstract Thromboembolic complications are frequently associated with advanced cancer. Interestingly, one of the major initiators of blood coagulation, tissue factor (TF), is reported to be overexpressed in several tumor types and can be found on both tumor cells and tumor vasculature. Although the exact mechanisms have yet to be elucidated, TF expressed on tumor cells can trigger intracellular signaling events through various pathways that can lead to tumor angiogenesis, proliferation, and metastasis. There exists preclinical evidence that disruption of TF dependent signaling can effectively inhibit tumor cell migration, metastasis, and angiogenesis. Here, we report for the first time that an antibody to tissue factor can also prevent tumor growth in vivo. Prophylactic administration of CNTO 859, a humanized anti-human TF antibody, was shown to inhibit experimental lung metastasis of MDA-MB-231 human breast carcinoma cells by over 99% compared to a control antibody. Furthermore, therapeutic doses of CNTO 859 were shown to reduce tumor incidence and growth of orthotopically implanted MDA-MB-231 cells. © 2006 Wiley-Liss, Inc. [source]

    Tight control of transgene expression by lentivirus vectors containing second-generation tetracycline-responsive promoters

    THE JOURNAL OF GENE MEDICINE, Issue 6 2005
    Krzysztof Pluta
    Abstract Background The goal of this study was to design improved regulatable lentivirus vector systems. The aim was to design tetracycline (tet)-regulatable lentivirus vectors based on the Tet-on system displaying low background expression in the absence of the doxycycline (DOX) inducer and high transgene expression levels in the presence of DOX. Methods We constructed a binary lentivirus vector system that is composed of a self-inactivating (SIN) lentivirus vector bearing inducible first- or second-generation tet-responsive promoter elements (TREs) driving expression of a transgene and a second lentivirus vector encoding a reverse tetracycline-controlled transactivator (rtTA) that activates transgene expression from the TRE in the presence of DOX. Results We evaluated a number of different rtTAs and found rtTA2S -M2 to induce the highest levels of transgene expression. Regulated transgene expression was stable in human breast carcinoma cells implanted into nude mice for up to 11 weeks. In an attempt to minimize background expression levels, the chicken ,-globin cHS4 insulator element was cloned into the 3, long terminal repeat (LTR) of the transgene transfer vector. The cHS4 insulator element reduced background expression but expression levels following DOX addition were lower than those observed with vectors lacking an insulator sequence. In a second strategy, vectors bearing second-generation TREs harboring repositioned tetracycline operator elements were used. Such vectors displayed greatly reduced leakiness in the absence of DOX and induced transgene expression levels were up to 522-fold above those seen in the absence of DOX. Conclusions Inducible lentivirus vectors bearing insulators or second-generation TREs will likely prove useful for applications demanding the lowest levels of background expression. Copyright © 2005 John Wiley & Sons, Ltd. [source]