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Session X : Cell death in cancer Poster X, 105 Significant co-expression of GLUT-1, Bcl-xl and Bax in colorectal cancer. Andrzej Wincewicz, Mariola Sulkowska, Mariusz Koda, Luiza Kanczuga-Koda, Stanislaw Sulkowski. Department of Pathology, Medical University of Bialystok, Waszyngtona 13, 15-269 Bialystok, Poland. E-mail: sulek@zeus.amb.edu.pl Hypoxic cancer cells overexpress GLUT-1 (Glucose transporter 1) to accelerate glucose intake mainly for low effective, anaerobic respiration, so that they wouldn’t die of oxygen deficiency. Ischemic cell injury triggers apoptosis. Regulators of cell suicide like Bax and Bcl-xl combine their functions to cause apoptosis or to rescue cells from death. GLUT-1, Bax and Bcl-xl are of prognostic significance in colorectal cancer but they have not been compared, yet. Thus, we aimed to determine eventual correlations between GLUT-1, Bax and Bcl-xl in association with different clinicopathological features of colorectal cancer patients. Expressions of the proteins were evaluated in specimens of 150 colorectal patients by immunohistochemistry with appliance of specific antibodies. The levels of tissue expressions were statistically analyzed with Spearman’s correlation test. Similarly to all the patients, GLUT-1 matched Bcl-xl and Bax in statistically significant manner regardless node involvement, grade of histological differentiation, histopathological type, tumor site, sex and age of patients. GLUT-1 correlated highly with Bcl-xl in both T2 and T3 tumors (p
Session X : Cell death in cancer Poster X, 106 Impact of Rb knock down on the modulation erufosine signal transduction in human leukemia cells Maya M. Zaharieva1,2, Milen Kirilov2, Minqiang Chai2, Stefan Berger3, Spiro M. Konstantinov1,2, Martin R. Berger2 1Faculty of Pharmacy, Medical University of Sofia, 2 Dunav Str, 1000 Sofia, Bulgaria 2German Cancer Research Center, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany 3Central Institute for Mental Help, Department of Molecular Biology, J5, 68 159 Mannheim The retinoblastoma gene Rb1 is a prototypical tumour supressor. Consistent with its tomoursupressor function Rb is known to inhibit proliferation. Recent studies indicate its role in suppressing apoptosis, too. Loss of Rb sensitizes cells to apoptosis, but loss of Rb can only contribute to tumor development under conditions in which apoptosis response is already compromised. The new alkylphosphocholine erufosine is an inductor of Rb in leukemic cells. Therefore, we decided to suppress the expression of RB using conventional phosphorotioate antisense oligonucleotides and siRNAs. Unfortunately, both types of oligonucleotides used didn’t cause stable and reproducible knock-down and we initiated viral transfection experiments for stable Rb knock-down in SKW-3, BV-173 and K-562 cells. The antisense sequence was firstly cloned in the pSUPER vector and tested on HEK 293T cells. For normalizing the transfection efficiency an EGFP-expressing vector was used in addition. To realize the transfer of the H1-shRNA cassette directed to the Rb-mRNA, the cells were infected with LentiLox virus which co-express an EGFP-protein. The resulting levels of target mRNA were measured by real-time RT-PCR after excluding of non-fluorescent cells by flow cytometry and cell sorting. The highest decrease of the Rb-mRNA (about 86%) was found in SKW-3 cells. A concomitent knock-down at the protein level was evidenced by Western blotting. The proliferation activity of the infected cells was estimated by colorimetric MTTdye reduction assay before and after erufosine treatment. Comparison of Rb knock-down and wild type leukemic cells revealed the presence of significant differences in cell cycle duration and sensitivity to erufosine, thus confirming the impact of Rb modulation for the mode of action of alkylphosphocholines which are known as promising antineoplastic signal transduction modulators. - 439 -
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- 1 - Luxembourg, January 25th to 2
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Table of content PREFACE ..........
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Preface In 1998, we organized the f
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Acknowledgments This meeting has be
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Group B (15h00 - 17h00) Session V.
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- 11 - Exhibition
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Visit our Expo (in alphabetical ord
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Thursday January 26th, 2006 (Early
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Thursday January 26th, 2006 (Evenin
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Regulation of inflammation and gluc
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Saturday January 28th, 2006 (Early
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Oral presentations (by alphabetical
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4: : Lottin S, Vercoutter-Edouart A
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the B-Raf/mitogen-activated/extrace
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Albertini MC, Accorsi A, Citterio B
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AP-1-dependent gene expression in s
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Jaks and cytokine receptors - an in
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The Role of Met-Gab1 Signalling in
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The mammalian tumor suppressor Scri
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SIGNAL TRANSDUCTION BY STRESS-ACTIV
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Title to be announced Caroline Dive
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Mechanisms of DNA methylation in ma
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Blocking the "4 Integrin-Paxillin I
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Regulation of NF-kB-dependent trans
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The immunomodulator AS101 induces g
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Signaling pathways leading to the a
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Boute, N., Jockers, R. and Issad, T
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Jespsen JS, Sorensen MD and Wengel
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8. Nishikawa, H., Kawai, K., Tanaka
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9) Proteome analysis of rat pancrea
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MicroRNA is an anti-apoptotic facto
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Resveratrol inhibits phorbol ester-
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Cross-talk between angiotensin II a
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Multiple role of histamine H 1 rece
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PI3K Targeting by the Beta-GBP Cyto
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D.P. Chopra, R.E. Menard, J. Janusz
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[2] Meijer, L., Flajolet, M. and Gr
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[4] Niemand, C., Nimmesgern, A., Ha
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Oncogenic signaling by mutant p53 M
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activity of the Peroxisome Prolifer
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Restauration of SHIP-1 activity in
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Hypoxia Signaling. Impact on Tumor
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5. Sokolov EI, Zykov KA, Pukhalsky
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HOW ANTITOXIC AND ANTICANCER AGENTS
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Listeria monocytogenes induced Rac1
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Epigenetic Regulation of Stem Cell
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Survey on in vitro cell death induc
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Distinct roles of IRF-3 and IRF-7 i
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Redox-Sensitive Transcription Facto
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Epigenic control of MHC2TA transcri
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Attenuation of MSK1-driven NF-kB ge
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Talking to chromatin: Silencers Sil
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Ubiquitin ligase Smurf1 controls os
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Workshop presentations (by alphabet
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Ambion MicroRNAs (miRNAs) are small
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Organizer: BIOBASE GmbH Date: Janua
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Reliable and efficient gene Knock-d
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Exploring ubiquitin signaling with
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Poster presentations Poster are cla
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Session I : protein domains Poster
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Session II. Receptor signaling and
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Session II : Receptor signaling and
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Session III. Protein kinase cascade
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Session III : Protein kinase cascad
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Session IV. Protein kinase inhibito
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IV. Protein kinase inhibitors: insi
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IV. Protein kinase inhibitors: insi
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V. Phosphatases as key cell signali
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VI. Proteasome degradation pathways
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VI. Proteasome degradation pathways
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Session VII. Stem cell specific cel
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VIII. Inflammation specific signali
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Session IX. Novel compounds targeti
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Session X : Cell death in cancer -
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Session X : Cell death in cancer Po
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Session XIII : Cell signaling pathw
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Session XIV : Transcriptional and t
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Session XV : Reactive oxygen specie
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Session XVI : Chemopreventive agent
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Session XVII : Cell signaling in he
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Dr. Nassera Aouali L-1526 Luxembour
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Dr. Giordano Bianchi Clinic of inte
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Mrs. Isabel Burghardt Laboratory of
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Pr. Czeslaw Cierniewski 92-215 Lodz
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Dr. Mark Ginsberg Mail code 0726 92
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Dr. Jochen Hefl Division of Signal
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Mr. Jan Jepsen 2100 Copenhagen DNK
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Mr. Christoph Lahtz AG Tumorgenetik
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Mrs. Rasa Merzvinskyte Department o
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Mr. Gustav Nilsonne Department of L
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Mrs. Christel Péqueux Tumour and D
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Dr. Gabriella Regis Tumor Immunolog
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