The Experts below are selected from a list of 6009 Experts worldwide ranked by ideXlab platform
Sami G Abdelhamide - One of the best experts on this subject based on the ideXlab platform.
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design synthesis and biological evaluation of novel quinazoLine derivatives as potential antitumor agents molecular docking study
European Journal of Medicinal Chemistry, 2010Co-Authors: Adel S Elazab, Mohamed A Alomar, Alaa A M Abdelaziz, Naglaa I Abdelaziz, Magda A A Elsayed, Abdulaziz M Aleisa, Mohamed M Sayedahmed, Sami G AbdelhamideAbstract:Abstract Novel derivatives of quinazoLine (1–27) have been synthesized and tested for their antitumor activity against three tumor Cell Lines among these Cell Lines the human Breast carcinoma Cell Line (MCF-7) in which EGFR is highly expressed. All tested compounds showed potent and selective activity against Breast cancer (MCF-7) with IC50 range of 3.35–6.81 μg/ml. With regarding broad-spectrum activity compounds 5, 9, 15, 18 and 20 exploited potent antitumor against human liver Cell Line (HEPG2), human Breast Cell Line (MCF-7) and human cervix Cell Line (HELA) with IC50 range of 3.35–5.59 μg/ml. Virtual screening was carried out through docking the designed compounds into the ATP binding site of epidermal growth factor receptor (EGFR) to predict if these compounds have analogous binding mode to the EGFR inhibitors.
Céline Galés - One of the best experts on this subject based on the ideXlab platform.
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Dosage-dependent regulation of Cell proliferation and adhesion through dual β2-adrenergic receptor/cAMP signals.
FASEB Journal, 2014Co-Authors: Ariana Bruzzone, Aude Saulière, Frédéric Finana, Jean-michel Sénard, Isabel Lüthy, Céline GalésAbstract:The role of β-adrenergic receptors (β-ARs) remains controversial in normal and tumor Breast. Herein we explore the cAMP signaling involved in β-AR-dependent control of proliferation and adhesion of nontumor human Breast Cell Line MCF-10A. Low concentrations of a β-agonist, isoproterenol (ISO), promote Cell adhesion (87.5% Cells remaining adherent to the plastic dishes following specific detachment vs. 35.0% in control, P
Edward J. Delikatny - One of the best experts on this subject based on the ideXlab platform.
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Induction of magnetic resonance-visible lipid in a transformed human Breast Cell Line by tetraphenylphosphonium chloride.
International Journal of Cancer, 1997Co-Authors: Sandrine K. Roman, Rebecca L. Hancock, Thomas M. Jeitner, Darryl C. Rideout, Wendy A. Cooper, Edward J. DelikatnyAbstract:Proton magnetic resonance spectroscopy (1H MRS) and DNA flow cytometry were used to monitor the effects of the cationic lipophilic phosphonium salt and potential antineoplastic agent tetraphenylphosphonium chloride (TPP) on the transformed human Breast Cell Line HBL-100. TPP treatment for 48 hr was cytostatic at low concentrations and cytotoxic at higher concentrations with an IC50 of 55 μM as measured by Trypan blue exclusion. At micromolar concentrations, TPP caused a significant increase in the methylene MR signal arising from mobile lipid as measured by the ratio of the lipid CH2 peak height to either the CH3 peak height (internal referencing) or the peak height for p-aminobenzoic acid (PABA) as an external reference in a co-axial capillary within the sample. Over the same concentration range, TPP caused a slowing of passage through S phase as demonstrated by a significant depletion of Cells in G2/M phase with a concurrent but non-significant increase in Cells in S. Time-dependent increases in MR-visible lipid were observed with 2 μM TPP treatment, and the removal of TPP from the culture medium caused no significant reduction in mobile lipid. Two-dimensional 1H|Cv1H COSY spectra of TPP-treated HBL-100 Cells revealed concentration-dependent increases in cross-peak volume ratios arising from lipid acyl chains relative to both internal (lysine, polyamines) and external (PABA) standards. Increases in choLine and glycerophosphochoLine cross-peak volume ratios were observed, indicating that the catabolism or rearrangement of phospholipids may be responsible for the observed MR-visible lipid increases. Int. J. Cancer 73:570–579, 1997. © 1997 Wiley-Liss, Inc.
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Tetraphenylphosphonium chloride induced mr-visible lipid accumulation in a malignant human Breast Cell Line
International Journal of Cancer, 1996Co-Authors: Edward J. Delikatny, Sandrine K. Roman, Rebecca L. Hancock, Thomas M. Jeitner, Catherine M. Lander, Darryl C. Rideout, Carolyn E. MountfordAbstract:The effect of the cationic lipophilic phosphonium salt tetraphenylphosphonium chloride (TPP) on a human malignant Breast Cell Line, DU4475, was monitored with proton nuclear magnetic resonance ( 1 H MRS). TPP caused a dose- and time-dependent increase in resonances arising from MR-visible lipid as measured by the CH 2 /CH 3 ratio in the 1-dimensional 1 H MR spectrum. Two-dimensional MRS identified increases in the glycerophosphochoLine/lysine cross-peak ratio and corresponding decreases in the phosphochoLine/lysine ratio in a dose-dependent fashion in TPP-treated Cells. Lipid metabolic changes are discussed in the light of other MR experiments, and the data indicate that accumulation of MR-visible lipids may arise from the rearrangement of phospholipids accompanying mitochondrial destruction or from the catabolism of phospholipids associated with early events in the cytotoxic process.
Ahmed Ahidouch - One of the best experts on this subject based on the ideXlab platform.
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K^+ Channel Expression in Human Breast Cancer Cells: Involvement in Cell Cycle Regulation and Carcinogenesis
Journal of Membrane Biology, 2008Co-Authors: Halima Ouadid-ahidouch, Ahmed AhidouchAbstract:K^+ channels are a most diverse class of ion channels in the plasma membrane and are distributed widely throughout a variety of Cells including cancer Cells. Evidence has been accumulating from fundamental studies indicating that tumour Cells possess various types of K^+ channels and that these K^+ channels play important roles in regulating tumor Cell proliferation, Cell cycle progression and apoptosis. Moreover, a significant increase in K^+ channel expression has been correlated with tumorigenesis, suggesting the possibility of using these proteins as transformation markers and perhaps reducing the tumor growth rate by selectively inhibiting their functional activity. Significant progress has been made in defining the properties of Breast K^+ channels, including their biophysical and pharmacological properties and distribution throughout different phases of the Cell cycle in Breast Cell Line MCF-7. This review aims to provide a comprehensive overview of the current state of research into K^+ channels/currents in Breast cancer Cells. The possible mechanisms by which K^+ channels affect tumor Cell proliferation and Cell cycle progression are discussed.
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k channel expression in human Breast cancer Cells involvement in Cell cycle regulation and carcinogenesis
The Journal of Membrane Biology, 2008Co-Authors: Halima Ouadidahidouch, Ahmed AhidouchAbstract:K+ channels are a most diverse class of ion channels in the plasma membrane and are distributed widely throughout a variety of Cells including cancer Cells. Evidence has been accumulating from fundamental studies indicating that tumour Cells possess various types of K+ channels and that these K+ channels play important roles in regulating tumor Cell proliferation, Cell cycle progression and apoptosis. Moreover, a significant increase in K+ channel expression has been correlated with tumorigenesis, suggesting the possibility of using these proteins as transformation markers and perhaps reducing the tumor growth rate by selectively inhibiting their functional activity. Significant progress has been made in defining the properties of Breast K+ channels, including their biophysical and pharmacological properties and distribution throughout different phases of the Cell cycle in Breast Cell Line MCF-7. This review aims to provide a comprehensive overview of the current state of research into K+ channels/currents in Breast cancer Cells. The possible mechanisms by which K+ channels affect tumor Cell proliferation and Cell cycle progression are discussed.
Felix Broecker - One of the best experts on this subject based on the ideXlab platform.
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transcriptional signature induced by a metastasis promoting c src mutant in a human Breast Cell Line
FEBS Journal, 2016Co-Authors: Felix Broecker, Christopher Hardt, Ralf Herwig, Bernd Timmermann, Martin Kerick, Andrea Wunderlich, Michal R Schweiger, Lubor Borsig, Mathias HeikenwalderAbstract:Deletions at the C-terminus of the proto-oncogene protein c-Src kinase are found in the viral oncogene protein v-Src as well as in some advanced human colon cancers. They are associated with increased kinase activity and Cellular invasiveness. Here, we analyzed the mRNA expression signature of a constitutively active C-terminal mutant of c-Src, c-Src(mt), in comparison with its wild-type protein, c-Src(wt), in the human non-transformed Breast epithelial Cell Line MCF-10A. We demonstrated previously that the mutant altered migratory and metastatic properties. Genome-wide transcriptome analysis revealed that c-Src(mt) de-regulated the expression levels of approximately 430 mRNAs whose gene products are mainly involved in the Cellular processes of migration and adhesion, apoptosis and protein synthesis. 82.9% of these genes have previously been linked to Cellular migration, while the others play roles in RNA transport and splicing processes, for instance. Consistent with the transcriptome data, Cells expressingc-Src(mt), but not those expressing c-Src(wt), showed the capacity to metastasize into the lungs of mice in vivo. The mRNA expression profile of c-Src(mt)-expressing Cells shows significant overlap with that of various primary human tumor samples, possibly reflecting elevated Src activity in some cancerous Cells. Expression of c-Src(mt) led to elevated migratory potential. We used this model system to analyze the transcriptional changes associated with an invasive Cellular phenotype. These genes and pathways de-regulated by c-Src(mt) may provide suitable biomarkers or targets of therapeutic approaches for metastatic Cells.This project was submitted to the National Center for Biotechnology Information BioProject under ID PRJNA288540. The Illumina RNA-Seq reads are available in the National Center for Biotechnology Information Sequence Read Archive under study ID SRP060008 with accession numbers SRS977414 for MCF-10A Cells, SRS977717 for mock Cells, SRS978053 for c-Src(wt) Cells and SRS978046 for c-Src(mt) Cells.
