Navegando por Palavras-chave "Epidermal growth factor"
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- ItemSomente MetadadadosAdhesion Molecules Affected by Treatment of Lung Cancer Cells with Epidermal Growth Factor(Springer, 2011-10-01) Fonseca, Fernando L. A. [UNIFESP]; Azzalis, Ligia A. [UNIFESP]; Feder, David; Nogoceke, Everson; Junqueira, Virginia B. C. [UNIFESP]; Valenti, Vitor E.; Abreu, Luiz Carlos de; Fac Med ABC; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP); Roche Ctr Med GenomLung cancer is one of the leading causes of death in the world. Some tumor events are attributed to an important group of molecules (cadherins and integrins). We evaluated the interactions of cell adhesion molecules in cell lines from lung cancer. Two lung cancer cell lines were nonmetastatic (H358 and H441) and two were metastatic (H1299 and H292). All cell lines were treated with epidermal growth factor (EGF), and Western blot analysis was performed to assess the interactions between these proteins. the bronchoalveolar cells H358 showed the three analyzed proteins: E-cadherin, beta-catenin, and p120 catenin. the adenocarcinoma cells H441 did not present p120 catenin, and carcinoma cells did not show E-cadherin (H1299) or p120 catenin (H292). FAK (pTyr925) was dephosphorylated in adenocarcinoma cells H441, absent in carcinoma cells H1299, and upregulated in the other carcinoma cells H292. p130Cas showed no difference when the cell lines were treated with EGF for 30 min; it was absent in the metastatic carcinoma cells H1299. Paxillin was dephosphorylated in adenocarcinoma cells H441 and also absent in other metastatic carcinoma cells H292. Vinculin showed the same results, and talin was downregulated in adenocarcinoma cells H441 when the cells were treated with EGF. Rap1 was downregulated and PYK2 was upregulated in the same cell line. Our data help to comprehend the mechanism involved in cell migration to the blood and metastasis generation. in conclusion, the expression patterns of cell-cell adhesion were not affected by EGF treatment but it affected cell-extracellular matrix adhesion.
- ItemAcesso aberto (Open Access)Protein expression of VEGF, IGF-1 and FGF in retroocular connective tissues and clinical correlation in Graves' ophthalmopathy(Conselho Brasileiro de Oftalmologia, 2008-08-01) Matos, Kimble [UNIFESP]; Manso, Paulo Gois [UNIFESP]; Marback, Eduardo [UNIFESP]; Furlanetto, Reinaldo [UNIFESP]; Alberti, Gustave Nosé; Nosé, Vania [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Federal da Bahia; Tufts University Medical Center; Brigham and Women's Hospital Department of PathologyPURPOSE: To investigate the immunohistochemical expression (IGF-1, EGFr, EGF, c-erbB-2/HER-2/neu, PDGF-A, PDGF-B, FGF and VEGF) in patients with Graves' ophthalmopathy. METHODS: Twenty-four samples (Graves' ophthalmopathy patients) underwent lateral rectus muscle and surrounding fibrous and adipose tissue biopsy. The control group was obtained by strabismus surgery. Correlation between clinical- ophthalmologic, endocrinological, ultrasonographic findings, and immunohistochemical expression was performed. RESULTS: IGF-1: There were 7 positive cases (29.2%). There was a direct relation with higher CAS (clinical activity score) in all of them and if only CAS equal or higher than 5 was considered, this was 54.5%. FGF: There was expression in 5 cases (20.8%) with a direct relation in all those with higher CAS (>5) (45.4%). VEGF: There were two positive cases (8.3%) for VEGF in endothelial cells, in these cases the patients also presented CAS higher than 5. There was no expressions of all growth factors in the control group. CONCLUSIONS: All patients, except one, with positive expression of FGF, IGF-1 and VEGF showed CAS greater than 5, suggesting in this way an important role of these growth factors in the pathogenesis and severity of Graves' ophthalmopathy. However, statistical analysis revealed only significant association between IGF-1 and male sex (P=0.034). Low ultrasound reflectivity and endocrine status may not correlate directly with disease activity or with immunoexpression of growth factors and c-erbB-2/HER-2/neu.
- ItemSomente MetadadadosProtein tyrosine phosphatase alpha regulates cell detachment and cell death profiles induced by nitric oxide donors in the A(431) human carcinoma cell line(Maney Publishing, 2011-01-01) Costa, Paulo E. da [UNIFESP]; Batista, Wagner L. [UNIFESP]; Curcio, Marli F. [UNIFESP]; Moraes, Miriam S. [UNIFESP]; Borges, Roberta Eller [UNIFESP]; Nascimento, Patricia A. [UNIFESP]; Travassos, Luiz R. [UNIFESP]; Monteiro, Hugo P. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)We investigated the role of protein tyrosine phosphatase-alpha (PTP alpha) expression in the cell death profile of the A431 human carcinoma cell line that was induced by cytotoxic concentrations of the nitric oxide (NO) donors sodium nitroprusside (SNP) and 3,3-bis-(aminoethyl)-1-hydroxy-2-oxo-1-triazene (NOC-18). Both NO donors promoted extensive cell detachment in A431 parental cells as compared to the detachment observed for A431 cells that ectopically expressed PTP alpha (A431 (A27B(PTP alpha)) cells). the NO-induced cell death characteristics for both cell lines were examined. After incubation for 10 hours with 2.0 mM SNP, attached or detached A431 cells underwent apoptosis. Cells were highly positive for Annexin-V, featured increased cleavage of procaspase-8, activation of downstream caspase-3, and activation of poly-ADP-ribose polymerase 1 (PARP-1). in contrast, exposure of A431 (A27B(PTP alpha)) cells to 2.0 mM SNP produced an increase in the release of lactate dehydrogenase and enhanced incorporation of propidium iodide. in addition, A431 (A27B(PTP alpha)) cells showed partial inhibition of the activities of caspase-8, caspase-3, and PARP-1 upon detachment and cell death induced by SNP treatment. Results indicate that necrotic cell damage was induced, characterized by cellular swelling and lysis. We conclude from these results that PTP alpha regulates the A431 tumor cell death profile mediated by NO donors. Expression of PTP alpha or its absence may determine the occurrence of NO-induced cell death with necrotic or apoptotic features, respectively.