poster abstracts

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Constance Oliver. Klaus Hartfelder. Sang Won Han. Edna Kimura. Luiz Renato França. Sérgio Schenckman. Emer Suavinho Ferro. Manoel Costa. Silvana Allodi.
POSTER ABSTRACTS

July 25th- 28th, 2012 | Rio de Janeiro, Brazil Co-Organizers

The Brazilian Society for Cell Biology (SBBC) Executive committee President Vice-President Directors

Secretary Treasurer

Wilson Savino - Fiocruz, Rio de Janeiro Vilma R Martins – Hospital A C Camargo, São Paulo Marimélia Porcionatto - UNIFESP, São Paulo Patrícia Gama - USP, São Paulo Flavia A C Gomes - UFRJ, Rio de Janeiro Irene Yan - USP, São Paulo Marinilce F Santos - USP, São Paulo

The International Federation for Cell Biology (IFCB) President Vice-President Secretary General

Denys Wheatley - Aberdeen, Scotland, UK Cheng-Wen Wu - NHRI, Taiwan Hernandes F Carvalho - UNICAMP, Brazil

Financial Support

FCW Fundação Conrado Wessel

Institutional Support

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Organizing Committee Co-Chairs Hernandes F Carvalho (State University of Campinas) International Federation for Cell Biology IFCB Patrícia Gama (University of São Paulo) Brazilian Society for Cell Biology SBBC Brazilian Committee Estela Bevilacqua (University of São Paulo) Flávia Gomes (Federal University of Rio de Janeiro) Irene Yan (University of São Paulo) Marinilce F Santos (University of São Paulo) Marimélia Porcionatto (Federal University of São Paulo) Milton Moraes (FIOCRUZ) Thereza Christina Barja-Fidalgo (University of Rio de Janeiro)

International Contacts Europe: Anne Eichmann (College de France, France; Yale University, USA) US: Bechara Kachar (NIDCD, NIH, USA) Latin America: Gabriel Rabinovitch (Buenos Aires University, Argentina) Asia: Ken Wen Wu (NHRI, Taiwan) Australia: James Armitage (Monash University, Australia)

Scientific Committee Bechara Kachar Betina Malnic Carla Collares Carlos Ramos Célia Regina Garcia Celuta Sales Alviano Cláudia Mermelstein Claudio Simon Constance Oliver Edna Kimura Emer Suavinho Ferro Enilza Espreafico Estela Bevilacqua Fábio Papes Fernando Costa e Silva Filho Flávia CA Gomes Glaucia Santelli Gustavo Amarante Mendes

Hernandes F Carvalho Hugo Armelin Irene Yan Ivarne Tersariol Jorg Kobarg José Garcia Abreu José Mauro Granjeiro José Xavier Neto Klaus Hartfelder Luiz Renato França Manoel Costa Mari Sogayar Maria Célia Jamur Maria Isabel Cano Marimélia Porcionatto Marinilce F Santos Marlene Benchimol Mirian Jasulionis

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Nadja Souza-Pinto Paolo Meda Patrícia Bozza Patrícia Gama Renata Pasqualini Ricardo Guellerman Roger Chammas Ruy Jaeger Sang Won Han Sérgio Schenckman Silvana Allodi Vilma R Martins Vivaldo Moura Neto Wadih Arap Wanderley de Souza Wilma Kempinas Wilson Savino

Presentation guidelines Poster Sessions will be held at 1st and 2nd floors (Room 203) and will be organized according to the different areas. Please check your Board ID above. Poster Session I: Thursday, July 26th Set up: Wednesday 15h00- 17h00 and Thursday 9h00- 9h30 Tear down: until 15h30 Poster Session II: Friday, July 27th Set up: Thursday 16h30 -18h00 and Friday 9h00- 9h30 Tear down: 16h00- 16h30 Author presentation hour for both sessions: 11h45- 12h45 even numbers 12h45-13h45- odd numbers Poster numbers will identify the boards. Tapes and hangers should be brought to the area by presenters. The Organizing Committee will not provide these items and will not collect and keep Posters that are left on the Boards. We will invite our speakers to select and nominate three best posters according to their expertise. Winners and prizes will be announced during the closing cerimony

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B207 Analysis of the leptin signaling pathway components of thyroid papillary carcinoma of children and adolescents by immunostaining Authors: Mario Lucio Cordeiro Araujo Junior; Viviane Younes-Rapozo; Nayara PeixotoSilva; Patrícia Lisboa; Elaine de Oliveira; Rossana Corbo; Marcelli Gatto; Albanita Viana de Oliveira ; Egberto Gaspar de Moura Children and adolescents account for 2% of the thyroid carcinoma cases. The prognosis of papillary thyroid carcinoma is excellent with survival rates over 95% as long as they are diagnosed in early stages. Leptin can act as a mitogenic and angiogenic factor and there is a greater expression of leptin and/or its receptor (ObR) in several types of tumors, including papillary thyroid carcinoma in adults. Here, we evaluated the expression/distribution of components of leptin signaling cascade in samples of papillary carcinoma of children and adolescents. Histological sections of 53 patients with papillary thyroid carcinoma of National Cancer Institute – INCA (CE0029.0.007.000-11) were done for diagnosis review and confirmation of the papillary carcinoma, observing the presence of non-neoplastic adjacent thyroid tissue for comparison. Four samples were analyzed by immunofluorescence using the antibodies anti-ObR, anti-pJAK-2 and anti-pSTAT3. On the non-neoplastic tissue, the pattern of immunostaining for ObR, pJAK-2 and pSTAT3 was in a punctiform and perinuclear shape with a continuous and more homogeneous distribution along the membrane. In the papillary carcinoma, we observed a heterogeneous pattern with a stronger or concentrated immunoreactivity in certain regions, facing the fibrovascular core of the neoplastic papillas. We have shown that the leptin pathway displays a differentiated distribution on the papillary carcinoma of children and adolescents, facing the fibrovascular core, suggesting that leptin can contribute to tumoral growth and that the signaling study can help in the diagnosis and prognosis of the disease. Support: FAPERJ, CAPES, CNPq. Authors: 1-Mario Lucio Cordeiro Araujo Junior, [email protected] . Adress: Rua Capitão Cesar de Andrade, 168/505 Leblon, Rio de Janeiro/RJ CEP 22431-010. UERJ/INCA. (21)-87576760 2-Viviane Younes-Rapozo, [email protected], UERJ 3-Nayara Peixoto-Silva, [email protected], UERJ 4- Elaine de Oliveira, [email protected], UERJ 5-Patrícia Cristina Lisboa, [email protected], UERJ 6-Rossana Corbo, [email protected], INCA 7-Marcelli Gatto, [email protected], INCA 8-Albanita Viana de Oliveira, [email protected], UERJ 9-Egberto Gaspar de Moura, [email protected], UERJ

B208 Apoptosis induction by a new derivative of podophyllotoxin in HL-60 cells Faheina-Martins, G.V.1; Silveira, A.L1; Dantas, B.B. 1; Araújo, D.A.M1. 1 - Laboratório de Biotecnologia Celular e Molecular, Centro de Biotecnologia, UFPB, João Pessoa – PB, Brasil e-mail: [email protected] Celular: (83) 87175879 ou (83) 9993-2568 Fontes de Financiamento: CNPq Background: The suppression of apoptotic mechanisms is involved both in the process of tumorigenesis and maintenance of the malignant phenotype as in the development of drug resistance. Therefore, the development of compounds that induce apoptosis is one of the therapeutic strategies in the field of oncology. Aim: In this work, the cytotoxic effect of a new podophyllotoxin derivative was evaluated on HL-60 cell line. Methodology: To assess the type of cell death induced in HL-60, cells were incubated with the derivative A98 (4, 6 and 8 μM) for 1, 3, 6 and 12 hours. Etoposide (5 μM) was used as a positive control. Flow cytometry was performed for detection of phosphatidilserine exposure, determination of mitochondrial membrane potential and estimation of caspases -8, -9, and -3 activity. DNA fragmentation was qualitatively analyzed by gel electrophoresis. The expression of bcl-2 was evaluated by western blot. Results: Death promoted by derivative A398 was time and concentration-dependent. After a period of 1 hour, there was an increase in mitochondrial membrane depolarization and inhibition of the expression of Bcl-2. After 3 hours, derivative A398 induced externalization of phosphatidylserine, promoted significant activation of caspases -8, -9 and -3 and induced maximal DNA fragmentation in 6 hours. These effects are much faster than the one promoted by etoposide. Conclusions: Consistent with these observations, the drug could effectively induce early apoptosis in leukemia cells, through the activation of the extrinsic and intrinsic pathways of death.

B209 A new Fab inhibits cell proliferation in MCF7 breast carcinoma cells

B210 Induction of Apoptosis in human lung alveolar carcinoma epithelial cells (A549) by the metallic complex cis-Tetraammine(oxalato)Ruthenium(III) Dithionate

Thaise G. Araújo1; Cláudia M. Rodrigues1; Bruna F. Matias1; Yara C.P. Maia1, Angela A.S. Sena1; Carolina Fernandes Reis2; Carlos Ueira-Vieira1; Luiz R Goulart1 1 Laboratory of Nanobiotechnology, Institute of Genetics and Biochemistry – Federal University of Uberlandia. 2 Laboratory of Cancer Molecular Genetics, Faculty of Medical Sciences – UNICAMP, Address: 126, Tessália Vieira de Camargo St.,Zip code: 13083-887. Campinas-SP, Brazil. TGA: [email protected] CMR: [email protected] BFM: [email protected] YCPM: [email protected] AASS: [email protected] CFR: [email protected] CUV: [email protected] LRG: [email protected] Abstract Breast cancer is the most frequent malignant tumor of women in North America, is the second leading cause of death, after lung cancer and the parameters currently available are not sufficient to capture its individual complexity. However, a heterogeneous disease, encompassing a wide variety of pathological entities in which 40% of the patients still succumb, highlights the need for new therapeutic strategies and identification of new targets. We have constructed and selection a FabC4 recombinant antibody by phage display in search for antigen-specific binding without cross-reactivity, unequal expression of genes repertoire and yielding new applications in diagnosis and therapy. The human breast carcinoma cell line MCF7 was established to elucidate the functional role of FabC4. We carried out cell viability assay (MTT), Immunofluorescence and Proliferation analysis by flow cytometry, using the follow concentrations of the antibody: 0.87uM, 1.75uM, 3.5uM and 5.0uM. Confocal microscopy images revealed that FabC4 bounded to MCF7 cells. Under the experimental conditions used, the FabC4 did not influence cell growth but inhibit cell proliferation when used 5.0uM of the antibody. Our results suggest that FabC4 recognize a cytoplasmatic antigen which influences of cell division. This Fab marker selected by phage display in this investigation may be used in breast cancer therapy. Further analysis in other cells lines is necessary to elucidate the functions of this potential antibody marker for breast cancer diagnosis and treatment. Financial support: CAPES, CNPq, FAPEMIG

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ELISÂNGELA DE PAULA SILVEIRA-LACERDA1; FLÁVIA DE CASTRO PEREIRA1, ALINY PEREIRA DE LIMA1, WANESSA CARVALHO PIRES1, CESAR AUGUSTO SAM TIAGO VILANOVA-COSTA1 1

Laboratório de Genética Molecular e Citogenética, Instituto de Ciências Biológicas, UniversidadeFederal de Goiás - UFG, Goiânia, Goiás, Brazil. * [email protected] First-line treatment for patients with advanced non-small cell lung cancer (NSCLC) includes platinum compounds such cisplatin [cis-diamminedichloroplatinum(II)] and its analogues carboplatin and oxaliplatin. Ruthenium complexes have shown potential utility in chemotherapy. In the present work we studied the cytotoxic activity, cell cycle arrest and the induction of apoptosis of the compound of cisTetraammine(oxalato)Ruthenium(III) Dithionate against human lung carcinoma (A549) and normal human fetal lung fibroblast (MRC-5) cell lines. Results showed that this Ruthenium(III) complex causes a significant reduction of proliferation of A549 cells with viabilities ranging from 55.5% to 24.6% when treated with 40 µM for 24 and 48h; and 32% to 18.2% when treated with 150 µM for 24 and 48h. This complex induced a moderate (31.9% and 39.6% for concentrations 10 and 40 µM, respectively) to high degree (74% for concentration 150 µM) of cytotoxic activity against A549 cells (IC50= 33.72 µM). On the other hand, the normal lung fibroblast MRC-5 did not show significant reduction proliferation in the presence of the Ruthenium(III) complex. Even when treated with higher concentrations of the complex for 48 hours, MRC-5 cells showed viabilities ranging from 85% to 78,4% for 40 µM and 150 µM, respectively. Cell cycle analysis showed that the Ruthenium(III) complex led to an accumulation of A549 cells in G1 phase and increased Sub-G1. In addition, treatment with this complex induced apoptosis, as observed by the increased numbers of Annexin V-positive cells and increased mRNA expression of caspase-3. Keywords: cis-Tetraammine(oxalato)Ruthenium(III) Dithionate; citotoxic activity; A549; MRC-5; Lung cancer; apoptosis.