82 research outputs found

    The role of miRNA-133b and its target gene SIRT1 in FAP-derived desmoid tumor.

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    Signaling pathways have a key role in driving the uncontrolled development of familial adenomatous polyposis (FAP)- associated and sporadic desmoid tumors (DTs). The relationship between the Wnt/b-catenin signaling pathway and DTs has been extensively studied, but no reliable biomarkers able to detect their histological subtype have been identified for the accurate diagnosis. In this study we studied the differences in miRNA expression between sporadic (20 patients) and FAP-associated DTs (7 patients) using microarray confirmed by quantitative PCR (qPCR). The analysis showed 19 dysregulated miRNAs. Among them miR-133b levels were significantly lower in FAP-associated DT than in sporadic DT. Therefore, two mRNAs, associated to miR-133b and β-catenin expression, the SIRT1 and ELAVL1were analyzed. The qPCR analysis showed that SIRT1 mRNA levels were significantly up-regulated in FAP-associated DT than in sporadic DT, whereas no differences in ELAVL1 expression was observed between these two DT types. In addition, a negative correlation was observed between miR-133b and SIRT1 in FAP-associated DTs, but not in sporadic DTs. The miR-133b-SIRT1-β-catenin axis may represent a novel mechanism underlying progression of FAP-associated D

    The omega rho pi coupling in the VMD model revisited

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    We determine the value of the \omega -\rho- \pi mesons coupling (g_{\omega\rho\pi}), in the context of the vector meson dominance model, from radiative decays, the \omega \rightarrow 3\pi decay width and the e^+e^- \rightarrow 3\pi cross section. For the last two observables we consider the effect of either a heavier resonance (\rho'(1450)) or a contact term. A weighted average of the results from the set of observables yields g_{\omega\rho\pi} =14.7 \pm 0.1 GeV^{-1} in absence of those contributions, and g_{\omega\rho\pi} =11.9 \pm 0.2 GeV^{-1} or g_{\omega\rho\pi} =11.7 \pm 0.1 GeV^{-1} when including the \rho' or contact term respectively. The inclusion of these additional terms makes the estimates from the different observables to lay in a more reduced range. Improved measurements of these observables and the \rho'(1450) meson parameters are needed to give a definite answer on the pertinence of the inclusion of this last one in the considered processes.Comment: 14 pages, 5 figures. Extended analysis including SND and CMD2 data. References added. Matches published versio

    Quaternionic potentials in non-relativistic quantum mechanics

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    We discuss the Schrodinger equation in presence of quaternionic potentials. The study is performed analytically as long as it proves possible, when not, we resort to numerical calculations. The results obtained could be useful to investigate an underlying quaternionic quantum dynamics in particle physics. Experimental tests and proposals to observe quaternionic quantum effects by neutron interferometry are briefly reviewed.Comment: 21 pages, 16 figures (ps), AMS-Te

    Growth of a human mammary tumor cell line is blocked by galangin, a naturally occurring bioflavonoid, and is accompanied by down-regulation of cyclins D3, E, and A

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    INTRODUCTION: This study was designed to determine if and how a non-toxic, naturally occurring bioflavonoid, galangin, affects proliferation of human mammary tumor cells. Our previous studies demonstrated that, in other cell types, galangin is a potent inhibitor of the aryl hydrocarbon receptor (AhR), an environmental carcinogen-responsive transcription factor implicated in mammary tumor initiation and growth control. Because some current breast cancer therapeutics are ineffective in estrogen receptor (ER) negative tumors and since the AhR may be involved in breast cancer proliferation, the effects of galangin on the proliferation of an ER(-), AhR(high )line, Hs578T, were studied. METHODS: AhR expression and function in the presence or absence of galangin, a second AhR inhibitor, α-naphthoflavone (α-NF), an AhR agonist, indole-3-carbinol, and a transfected AhR repressor-encoding plasmid (FhAhRR) were studied in Hs578T cells by western blotting for nuclear (for instance, constitutively activated) AhR and by transfection of an AhR-driven reporter construct, pGudLuc. The effects of these agents on cell proliferation were studied by (3)H-thymidine incorporation and by flow cytometry. The effects on cyclins implicated in mammary tumorigenesis were evaluated by western blotting. RESULTS: Hs578T cells were shown to express high levels of constitutively active AhR. Constitutive and environmental chemical-induced AhR activity was profoundly suppressed by galangin as was cell proliferation. However, the failure of α-NF or FhAhRR transfection to block proliferation indicated that galangin-mediated AhR inhibition was either insufficient or unrelated to its ability to significantly block cell proliferation at therapeutically relevant doses (IC(50 )= 11 μM). Galangin inhibited transition of cells from the G(0)/G(1 )to the S phases of cell growth, likely through the nearly total elimination of cyclin D3. Expression of cyclins A and E was also suppressed. CONCLUSION: Galangin is a strong inhibitor of Hs578T cell proliferation that likely mediates this effect through a relatively unique mechanism, suppression of cyclin D3, and not through the AhR. The results suggest that this non-toxic bioflavonoid may be useful as a chemotherapeutic, particularly in combination with agents that target other components of the tumor cell cycle and in situations where estrogen receptor-specific therapeutics are ineffective
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