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Search Results: 1 - 10 of 1154 matches for " Sonja Eberth "
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The Wnt Pathway Target Gene CCND1 Changes Mitochondrial Localization and Decreases Mitochondrial Activity in Colorectal Cancer Cell Line SW480  [PDF]
Annica Vlad-Fiegen, Natalie Veronika Freytag, Susanne Dorn, Oliver Müller, Sonja Eberth
Journal of Biosciences and Medicines (JBM) , 2016, DOI: 10.4236/jbm.2016.412017
Abstract: Mutations leading to constitutive activation of the Wnt pathway and its target genes are frequently observed in cancer. The Wnt pathway promotes cell proliferation and increasing evidence supports its role also in cancer cell metabolism. This study aims to elucidate the role of the Wnt/β-catenin target gene CCND1 in these processes in colorectal cancer. We analyzed whether knock-down of CCND1 affects cell cycle progression and energy metabolism in a colorectal cancer cell line. Down-regulation of CCND1 led to retardation of the cell cycle. The proportion of cells in the G0 phase increased, while the amount of cells in the S- and G2/M phase decreased. Interestingly, knock-down of CCND1 changed the perinuclear localization of mitochondria into a homogeneous distribution within the cytosol. In addition CCND1 knock-down led to an increase of the intracellular ATP level indicating that cyclin D1 reduced mitochondrial activity. Our findings suggest that in addition to its role in cell cycle regulation, the Wnt target gene CCND1 regulates mitochondrial localization and inhibits mitochondrial activity in colorectal cancer cells.
DNA methylation regulates expression of VEGF-R2 (KDR) and VEGF-R3 (FLT4)
Hilmar Quentmeier, Sonja Eberth, Julia Romani, Herbert A Weich, Margarete Zaborski, Hans G Drexler
BMC Cancer , 2012, DOI: 10.1186/1471-2407-12-19
Abstract: Real-time (RT) PCR analysis was performed to quantify KDR and FLT4 expression in some ninety leukemia/lymphoma cell lines, human umbilical vein endothelial cells (HUVECs) and dermal microvascular endothelial cells (HDMECs). Western blot analyses and flow cytometric analyses confirmed results at the protein level. After bisulfite conversion of DNA we determined the methylation status of KDR and FLT4 by DNA sequencing and by methylation specific PCR (MSP). Western blot analyses were performed to examine the effect of VEGF-C on p42/44 MAPK activation.Expression of KDR and FLT4 was observed in cell lines from various leukemic entities, but not in lymphoma cell lines: 16% (10/62) of the leukemia cell lines expressed KDR, 42% (27/65) were FLT4 positive. None of thirty cell lines representing six lymphoma subtypes showed more than marginal expression of KDR or FLT4. Western blot analyses confirmed KDR and FLT4 protein expression in HDMECs, HUVECs and in cell lines with high VEGF-R mRNA levels. Mature VEGF-C induced p42/44 MAPK activation in the KDR- /FLT4+ cell line OCI-AML1 verifying the model character of this cell line for VEGF-C signal transduction studies. Bisulfite sequencing and MSP revealed that GpG islands in the promoter regions of KDR and FLT4 were unmethylated in HUVECs, HDMECs and KDR+ and FLT4+ cell lines, whereas methylated cell lines did not express these genes. In hypermethylated cell lines, KDR and FLT4 were re-inducible by treatment with the DNA demethylating agent 5-Aza-2'deoxycytidine, confirming epigenetic regulation of both genes.Our data show that VEGF-Rs KDR and FLT4 are silenced by DNA methylation. However, if the promoters are unmethylated, other factors (e.g. transactivation factors) determine the extent of KDR and FLT4 expression.Vascular endothelial growth factors (VEGFs) and their corresponding receptors (VEGF-Rs) are important regulators of angiogenesis and lymphangiogensis. VEGF-A binds VEGF-R1 (FLT1) and VEGF-R2 (KDR). Both tyrosine kinase
BCR-ABL1-independent PI3Kinase activation causing imatinib-resistance
Hilmar Quentmeier, Sonja Eberth, Julia Romani, Margarete Zaborski, Hans G Drexler
Journal of Hematology & Oncology , 2011, DOI: 10.1186/1756-8722-4-6
Abstract: Five of 19 BCR-ABL1 positive cell lines were resistant to imatinib-induced apoptosis (KCL-22, MHH-TALL1, NALM-1, SD-1, SUP-B15). None of the resistant cell lines carried mutations in the kinase domain of BCR-ABL1 and all showed resistance to second generation TKI, nilotinib or dasatinib. STAT5, ERK1/2 and the ribosomal S6 protein (RPS6) are BCR-ABL1 downstream effectors, and all three proteins are dephosphorylated by imatinib in sensitive cell lines. TKI-resistant phosphorylation of RPS6, but responsiveness as regards JAK/STAT5 and ERK1/2 signalling were characteristic for resistant cell lines. PI3K pathway inhibitors effected dephosphorylation of RPS6 in imatinib-resistant cell lines suggesting that an oncogene other than BCR-ABL1 might be responsible for activation of the PI3K/AKT1/mTOR pathway, which would explain the TKI resistance of these cells. We show that the TKI-resistant cell line KCL-22 carries a PI3Kα E545G mutation, a site critical for the constitutive activation of the PI3K/AKT1 pathway. Apoptosis in TKI-resistant cells could be induced by inhibition of AKT1, but not of mTOR.We introduce five Philadelphia-chromosome positive cell lines as TKI-resistance models. None of these cell lines carries mutations in the kinase domain of BCR-ABL1 or other molecular aberrations previously indicted in the context of imatinib-resistance. These cell lines are unique as they dephosphorylate ERK1/2 and STAT5 after treatment with imatinib, while PI3K/AKT1/mTOR activity remains unaffected. Inhibition of AKT1 leads to apoptosis in the imatinib-resistant cell lines. In conclusion, Ph+ cell lines show a form of imatinib-resistance attributable to constitutive activation of the PI3K/AKT1 pathway. Mutations in PIK3CA, as observed in cell line KCL-22, or PI3K activating oncogenes may undelie TKI-resistance in these cell lines.Expression of the Philadelphia chromosome (Ph), resulting from fusion of the non-receptor tyrosine kinase ABL1 on chromosome 9 with BCR on chromosome 21
Epigenetic regulation of CD44 in Hodgkin and non-Hodgkin lymphoma
Sonja Eberth, Bj?rn Schneider, Andreas Rosenwald, Elena M Hartmann, Julia Romani, Margarete Zaborski, Reiner Siebert, Hans G Drexler, Hilmar Quentmeier
BMC Cancer , 2010, DOI: 10.1186/1471-2407-10-517
Abstract: We screened for TSG methylation using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) in 40 lymphoma-derived cell lines representing anaplastic large cell lymphoma, Burkitt lymphoma (BL), diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), Hodgkin lymphoma and mantle cell lymphoma (MCL) as well as in 50 primary lymphoma samples. The methylation status of differentially methylated CD44 was verified by methylation-specific PCR and bisulfite sequencing. Gene expression of CD44 and its reactivation by DNA demethylation was determined by quantitative real-time PCR and on the protein level by flow cytometry. Induction of apoptosis by anti-CD44 antibody was analyzed by annexin-V/PI staining and flow cytometry.On average 8 ± 2.8 of 24 TSG were methylated per lymphoma cell line and 2.4 ± 2 of 24 TSG in primary lymphomas, whereas 0/24 TSG were methylated in tonsils and blood mononuclear cells from healthy donors. Notably, we identified that CD44 was hypermethylated and transcriptionally silenced in all BL and most FL and DLBCL cell lines, but was usually unmethylated and expressed in MCL cell lines. Concordant results were obtained from primary lymphoma material: CD44 was not methylated in MCL patients (0/11) whereas CD44 was frequently hypermethylated in BL patients (18/29). In cell lines with CD44 hypermethylation, expression was re-inducible at mRNA and protein levels by treatment with the DNA demethylating agent 5-Aza-2'-deoxycytidine, confirming epigenetic regulation of CD44. CD44 ligation assays with a monoclonal anti-CD44 antibody showed that CD44 can mediate apoptosis in CD44+ lymphoma cells. CD44 hypermethylated, CD44- lymphoma cell lines were consistently resistant towards anti-CD44 induced apoptosis.Our data show that CD44 is epigenetically regulated in lymphoma and undergoes de novo methylation in distinct lymphoma subtypes like BL. Thus CD44 may be a promising new epigenetic marker for diagnosis and a potential therape
Fermi surface renormalization and quantum confinement in the two-coupled chains model
Eberth Correa,Alvaro Ferraz
Physics , 2013, DOI: 10.1140/epjb/e2014-40804-3
Abstract: We address the problem of the Fermi surface renormalization and the quantum confinement regime (QCR) in the two coupled chains model(TCCM) of spinless fermions. We perform a self-consistent calculation of the renormalization group(RG) flows of the renormalized TCCM couplings and quasiparticle weight. On top of that we take explicitly into account the renormalization of the Fermi surface. The flow of the difference of the renormalized Fermi wave vectors associated with the bonding and antibonding bands has a dramatic effect on the single particle spectrum. Although the quasiparticle amplitude is nullified already at intermediate coupling the QCR is only observed at strong coupling. The state associated with this regime has a charge gap and it is not a Luttinger liquid. In contrast, the Fermi liquid regime is stabilized by the umklapp "$g_2$--like" interactions at very weak coupling regime.
A functional generalization of the field-theoretical renormalization group approach for the single-impurity Anderson model
Hermann Freire,Eberth Corrêa
Physics , 2010,
Abstract: We apply a functional implementation of the field-theoretical renormalization group (RG) method up to two loops to the single-impurity Anderson model. To achieve this, we follow a RG strategy similar to that proposed by Vojta \emph{et al.} [Phys. Rev. Lett. \textbf{85}, 4940 (2000)], which consists of defining a soft ultraviolet regulator in the space of Matsubara frequencies for the renormalized Green's function. Then we proceed to derive analytically and solve numerically integro-differential flow equations for the effective couplings and the quasiparticle weight of the present model, which fully treat the interplay of particle-particle and particle-hole parquet diagrams and the effect of the two-loop self-energy feedback into them. We show that our results correctly reproduce accurate numerical renormalization group data for weak to slightly moderate interactions. These results are in excellent agreement with other functional Wilsonian RG works available in the literature. Since the field-theoretical RG method turns out to be easier to implement at higher loops than the Wilsonian approach, higher-order calculations within the present approach could improve further the results for this model at stronger couplings. We argue that the present RG scheme could thus offer a possible alternative to other functional RG methods to describe electronic correlations within this model.
Short-Range Order in a Flat Two-Dimensional Fermi Surface
Eberth Correa,Hermann Freire,A. Ferraz
Physics , 2005,
Abstract: We present the two-loop renormalization group (RG) calculations of all the susceptibilities associated with the two-dimensional flat Fermi surface with rounded corners (FS). Our approach follows our fermionic field theory RG method presented in detail earlier on. In one loop order our calculation reproduce the results obtained previously by other RG schemes. All susceptibilities diverge at some energy scale and the antiferromagnetic SDW correlations produce indeed the dominant instability in the physical system. In contrast, in two-loop order, for a given initial set of values of coupling constant regime only one of the susceptibilities at a time seems to diverge.
Breakdown of the Fermi-liquid regime in the 2D Hubbard model from a two-loop field-theoretical renormalization group approach
Hermann Freire,Eberth Correa,Alvaro Ferraz
Physics , 2007, DOI: 10.1103/PhysRevB.78.125114
Abstract: We analyze the particle-hole symmetric two-dimensional Hubbard model on a square lattice starting from weak-to-moderate couplings by means of the field-theoretical renormalization group (RG) approach up to two-loop order. This method is essential in order to evaluate the effect of the momentum-resolved anomalous dimension $\eta(\textbf{p})$ which arises in the normal phase of this model on the corresponding low-energy single-particle excitations. As a result, we find important indications pointing to the existence of a non-Fermi liquid (NFL) regime at temperature $T\to 0$ displaying a truncated Fermi surface (FS) for a doping range exactly in between the well-known antiferromagnetic insulating and the $d_{x^2-y^2}$-wave singlet superconducting phases. This NFL evolves as a function of doping into a correlated metal with a large FS before the $d_{x^2-y^2}$-wave pairing susceptibility finally produces the dominant instability in the low-energy limit.
Insulating spin liquid in the lightly doped two-dimensional Hubbard model
Hermann Freire,Eberth Correa,Alvaro Ferraz
Physics , 2005, DOI: 10.1103/PhysRevB.73.073103
Abstract: We calculate the charge compressibility and uniform spin susceptibility for the two-dimensional (2D) Hubbard model slightly away from half-filling within a two-loop renormalization group scheme. We find numerically that both those quantities flow to zero as we increase the initial interaction strength from weak to intermediate couplings. This result implies gap openings in both charge and spin excitation spectra for the latter interaction regime. When this occurs, the ground state of the lightly doped 2D Hubbard model may be interpreted as an insulating spin liquid as opposed to a Mott insulating state.
Renormalization group calculation of the uniform susceptibilities in low-dimensional systems
Hermann Freire,Eberth Correa,Alvaro Ferraz
Physics , 2006, DOI: 10.1088/0305-4470/39/25/S12
Abstract: We analyze the one-dimensional (1D) and the two-dimensional (2D) repulsive Hubbard models (HM) for densities slightly away from half-filling through the behavior of two central quantities of a system: the uniform charge and spin susceptibilities. We point out that a consistent renormalization group treatment of them can only be achieved within a two-loop approach or beyond. In the 1D HM, we show that this scheme reproduces correctly the metallic behavior given by the well-known Luttinger liquid fixed-point result. Then, we use the same approach to deal with the more complicated 2D HM. In this case, we are able to show that both uniform susceptibilities become suppressed for moderate interaction parameters as one take the system towards the Fermi surface. Therefore, this result adds further support to the interpretation that those systems are in fact insulating spin liquids. Later, we perform the same calculations in 2D using the conventional random phase approximation, and establish clearly a comparison between the two schemes.
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