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Session X : Cell death in cancer Poster X, 57 Wogonin, a plant flavone, potentiates etoposide-induced apoptosis in cancer cells Eibai Lee 1 , Riyo Enomoto 1 , Chie Suzuki 1 , Masataka Ohno 1 , Toshinori Ohashi 1 , Azusa Miyauchi 1 , Eriko Tanimoto 1 , Kaori Maeda 1 , Hiroyuki Hirano 2 , Toshio Yokoi 2 and Chiyoko Sugahara 1 1 Department of Pharmacology and 2 Department of Pharmaceutical Chemistry, Faculty of Pharmaceutical Sciences, Kobe Gakuin University, Ikawadani-cho, Nishi-ku, Kobe 651-2180 Japan. E-mail : elee@pharm.kobegakuin.ac.jp Etoposide, a podophylotoxin anticancer agent, induces apoptotic cell death in normal and cancer cells. Etoposide-induced apoptosis plays a role in not only anticancer effect but also adverse reaction such as myelosuppression. Since we have found that wogonin, a flavone found in Scutellaria baicalensis, suppresses thymocyte apoptosis induced by various compounds including etoposide, we examined the effect of this flavone on etoposide-induced apoptosis in cancer cells. Although wogonin itself hardly affected biochemical and morphological features of apoptosis in leukemia cells such as Jurkat and HL-60 cells, this flavone significantly potentiated etoposide-induced apoptosis in these cells. Similarly, wogonin accelerated etoposide-induced cell death in lung cancer cells. Since wogonin had no effect on the action of other anticancer agents such as 5-FU and cisplatin, this flavone seems to accelerate only apoptotic cell death induced by etoposide in cancer cells. These results suggest that the modification of etoposide-induced apoptosis by wogonin may be available to reduce the adverse reaction of this agent. - 390 -
Session X : Cell death in cancer Poster X, 58 Jpk, a novel cell death inducer, regulates the expression of Hoxa7 in F9 teratocarcinoma cells, but not during apoptosis Eun Young Lee and Myoung Hee Kim Department of Anatomy, Embryology Lab., Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Sodaemoongu Shinchondong 134, Seoul, 120-752, Korea. E-mail: nannaya1210@paran.com ; mhkim1@yumc.yonsei.ac.kr Increased expression of both Meis1 and Hox genes, such as Hoxa7 and –a9 has been characterized in several acute myeloid leukemia. Although the overexpression of Meis1 alone was shown to induce massive apoptosis, coexpression of Meis1 and Hox was reported to suppress the apoptosis, suggesting that Hox protein might participate in the apoptotic process. Jpk was isolated as a putative regulatory factor associating with the upstream regulatory sequence of murine Hoxa7. Since overexpression of Jpk caused apoptosis in bacteria as well as in eukaryotic cells, we tried to analyze the relationship between Jpk and Hoxa7 during apoptosis after confirming the regulatory effect of Jpk on the expression of Hoxa7 in F9 teratocarcinoma cells. For that purpose, an effector (pEGFP-Jpk) and reporter (pGL2-NM307) plasmid containing a luciferase gene under the 307 bp (NM307) of Hoxa7 upstream regulatory sequence were constructed. In the presence of Jpk (effector), luciferase activity was increased and this enhancement was decreased by siRNA against Jpk, suggesting that Jpk is a regulatory factor of Hoxa7. In order to see whether Jpk still regulate the expression of Hoxa7 during apoptosis, F9 cells were transiently transfected with pcDNA-Jpk, and analyzed the expression of Jpk, Hoxa7, and CHOP-10 using RT-PCR. Hoxa7 was not upregulated in the presence of Jpk whereas CHOP-10 was upregulated, indicating that the regulatory mechanism of Jpk on the expression of Hoxa7 might be different depending on the cell status; i. e., apoptotic or proliferative condition. - 391 -
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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 XI : Cell death and cardiov
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Session XI: Cell death and cardiova
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Session XII : Cell death and neurod
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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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Mr. Igotz Delgado Biochemistry 4894
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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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Pr. Young Min Kim Division of Biolo
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Mr. Christoph Lahtz AG Tumorgenetik
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Pr. Etta Livneh 84105 Beer Sheva IS
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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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Pr. Moncef ZOUALI Centre Viggo Pete
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