Visit our Expo - Redox and Inflammation signaling 2012

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Session X : Cell death in cancer Poster X, 75 The essential role of the mitochondria-dependent death signaling cascade in chemotherapy-induced potentiation of Apo2L/TRAIL cytotoxicity in cultured thoracic cancer cells: Amplified caspase 8 is indispensable for combination-mediated massive cell death. Dao M. Nguyen, Wen-Shuz Yeow, Rishindra M. Reddy, M. Firdos Ziauddin, Wilson Tsai, David S. Schrump. Section of Thoracic Oncology, Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Email address: dao_nguyen@nih.gov Chemotherapeutic drugs, regardless of their mechanism of action, sensitize cancer cells to Apo2L/TRAIL cytotoxicity in vitro and in vivo animal model. The molecular basis of this effect is diverse, ranging from modulation of the DISC activity to phenotypic alteration of the levels of anti-/pro-apoptotic proteins. We hypothesized that chemotherapeutic drugs, by altering the pro-apoptotic threshold of mitochondria, synergize with Apo2L/TRAIL to promote cytotoxicity via recruitment of the type II caspase activation cascade. Cisplatin, Paclitaxel, histone deacetylase inhibitors Trichostatin A or Valproic acid all sensitize multiple cultured thoracic cancer cells to Apo2L/TRAIL. Combining individual chemotherapeutics (at sublethal concentrations) with Apo2L/TRAIL results in 2- to >20-fold enhancement of cellular sensitivity to this ligand and massive synergistic induction of apoptosis (
Session X : Cell death in cancer Poster X, 76 Modulation of p53 transcriptional activity by PRIMA-1 and Pifithrin-alpha : effects on staurosporine-induced apoptosis of wild-type and mutated p53 epithelial cells. Magali Nicolier, Jean-François Charlot, Jean-Luc Prétet and Christiane Mougin. IFR133, EA 3181, Carcinogenèse épithéliale, UFR Médecine et Pharmacie, 19 rue Ambroise Paré, 25000 Besançon, France. Email : magali.nicolier@univ-fcomte.fr The p53, a specific DNA-binding transcription factor, triggers multiple biological responses including cell cycle arrest and apoptosis. Inactivation of p53 functions by mutations or by viral oncoproteins such as E6 from high risk papillomavirus (HPV) is a common event in many human cancers. New chemotherapeutic approaches consist in the restoration of apoptosis through refolding p53 mutants by PRIMA-1 (p53 reactivation and induction of massive apoptosis). As a result, PRIMA-1 restores the transcriptional activity of mutated p53 (p53mt). Anti-cancer therapies also damage surrounding normal tissues which highly express wild-type p53 (p53wt). That is why Pifithrin-alpha (p-fifty three inhibitor), a chemical inhibitor of p53wt, has been proposed as an adjunct to protect normal cells from otherwise lethal doses of chemo/radiotherapy. Recently, we argued for a major role of p53 in staurosporine (ST)-induced apoptosis of immortalized epithelial cells, according to p53 status (wt or mt) [Charlot et al., Apoptosis 2004]. Here, we investigated the effects of PRIMA-1 and Pifithrin-alpha on ST-induced apoptosis of 5 different immortalized cell lines with variable p53 status (p53wt HeLa HPV 18+ and CaSki HPV 16+ cells ; p53mt C33-A cells; p53-/- SaOs-2 cells) [Charlot, Nicolier et al., Apoptosis, in press]. As expected, PRIMA-1 has no effect on p53wt or p53-/- cells. On the other hand, it increases p21 and Bax expression, mitochondrial membrane potential dissipation and DNA fragmentation of p53mt cells. By contrast, Pifithrin-alpha does not modify ST-induced apoptosis of p53mt and p53-/- cells but readily decreases the apoptosis of cells harbouring a transcriptionnally active p53. These data strength the evidence that PRIMA-1 could increase ST efficiency in tumors with mutant p53. Moreover, Pifithrin-alpha could be used in combination with ST and PRIMA-1 to prevent side effects of anti-tumor therapies on healthy tissues. - 409 -
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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 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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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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Mr. Yoo-Cheol Song Laboratory of Gy
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Pr. Moncef ZOUALI Centre Viggo Pete
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