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3 results on '"Laura Alaniz"'

1. Antitumor effects of hyaluronic acid inhibitor 4-methylumbelliferone in an orthotopic hepatocellular carcinoma model in mice

Author

Jorge B. Aquino, Flavia Piccioni, Juan Bayo, Alberto Passi, Catalina Atorrasagasti, Mariana Garcia, Laura Alaniz, Guillermo Mazzolini, Ignacio T Piedra Buena, Manglio Rizzo, Andrés Rodriguez, Mariana Malvicini, Manuela Viola, and Nestor Kippes

Subjects
Liver Cancer, Male, Necrosis, Cirrhosis, CIENCIAS MÉDICAS Y DE LA SALUD, Carcinoma, Hepatocellular, Antineoplastic Agents, Apoptosis, carcinoma, Thioacetamide, Liver Cirrhosis, Experimental, Biochemistry, hyaluronan, Mice, Liver Neoplasms, Experimental, In vivo, Fibrosis, Cell Line, Tumor, medicine, Animals, Humans, Glucuronosyltransferase, Hyaluronic Acid, Cell Proliferation, Mice, Inbred C3H, 4-Methylumbelliferone, Chemistry, fibrosis, Otras Medicina Básica, Fibroblasts, medicine.disease, Tumor Burden, Medicina Básica, Hyaluronan Receptors, Liver, Hepatocellular carcinoma, Cancer research, Hepatic stellate cell, Liver Fibrosis, medicine.symptom, Drug Screening Assays, Antitumor, Liver cancer, Hyaluronan Synthases, Hymecromone, Neoplasm Transplantation
Abstract

Liver cirrhosis is characterized by an excessive accumulation of extracellular matrix components, including hyaluronan (HA). In addition, cirrhosis is considered a pre-neoplastic disease for hepatocellular carcinoma (HCC). Altered HA biosynthesis is associated with cancer progression but its role in HCC is unknown. 4-Methylumbelliferone (4-MU), an orally available agent, is an HA synthesis inhibitor with anticancer properties. In this work, we used an orthotopic Hepa129 HCC model established in fibrotic livers induced by thioacetamide. We evaluated 4-MU effects on HCC cells and hepatic stellate cells (HSCs) in vitro by proliferation, apoptosis and cytotoxicity assays; tumor growth and fibrogenesis were also analyzed in vivo. Our results showed that treatment of HCC cells with 4-MU significantly reduced tumor cell proliferation and induced apoptosis, while primary cultured hepatocytes remained unaffected. 4-MU therapy reduced hepatic and systemic levels of HA. Tumors systemically treated with 4-MU showed the extensive areas of necrosis, inflammatory infiltrate and 2-3-fold reduced number of tumor satellites. No signs of toxicity were observed after 4-MU therapy. Animals treated with 4-MU developed a reduced fibrosis degree compared with controls (F1-2 vs F2-3, respectively). Importantly, 4-MU induced the apoptosis of HSCs in vitro and decreased the amount of activated HSCs in vivo. In conclusion, our results suggest a role for 4-MU as an anticancer agent for HCC associated with advanced fibrosis. Fil: Piccioni, Flavia Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral; Argentina Fil: Malvicini, Mariana. Universidad Austral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina Fil: García, Mariana Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral; Argentina Fil: Rodriguez, Andrés. Universidad Austral; Argentina Fil: Atorrasagasti, María Catalina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Universidad Austral; Argentina Fil: Kippes, Néstor Fabián. Universidad Austral; Argentina Fil: Piedra Buena, Ignacio T.. Universidad Austral; Argentina Fil: Rizzo, Manglio Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral; Argentina Fil: Bayo Fina, Juan Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral; Argentina. Ministerio de Ciencia. Tecnología e Innovación Productiva. Agencia Nacional de Promoción Científica y Tecnológica; Argentina Fil: Aquino, Jorge Benjamin. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral; Argentina Fil: Viola, Manuela. Universitá degli Studi dell’Insubria; Italia Fil: Passi, Alberto. Universitá degli Studi dell’Insubria; Italia Fil: Alaniz, Laura Daniela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral; Argentina Fil: Mazzolini Rizzo, Guillermo Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral; Argentina

Published
2011

2. Hyaluronan oligosaccharides induce cell death through PI3-K/Akt pathway independently of NF-kappaB transcription factor

Author

Rosalía Agusti, Silvia E. Hajos, Elida Alvarez, Norma Sterín-Speziale, Carola Gallo-Rodriguez, Laura Alaniz, and Mariana Garcia

Subjects
anion exchange chromatography, Lymphoma, Cell, phosphatidylinositol 3,4,5 trisphosphate, Apoptosis, animal cell, cancer cell culture, Biochemistry, NF-κB, Wortmannin, chemistry.chemical_compound, Mice, Phosphatidylinositol 3-Kinases, hyaluronic acid, amperometry, 1-Phosphatidylinositol 3-Kinase, phosphatidylinositol 3 kinase, Hyaluronic Acid, HPAEC-PAD, enzyme inhibition, Cell Death, pH, article, NF-kappa B, P13-K, enzyme activity, immunoglobulin enhancer binding protein, wortmannin, medicine.anatomical_structure, priority journal, enzyme synthesis, hypothesis, Signal transduction, signal transduction, Signal Transduction, Programmed cell death, Hyaluronan oligomers, Biology, cell survival, Cell Line, Tumor, inhibition kinetics, medicine, oligosaccharide, Animalia, Animals, controlled study, Protein kinase B, mouse, nonhuman, Dose-Response Relationship, Drug, Phosphatidylinositol (3,4,5)-trisphosphate, Akt, NFKB1, Molecular biology, protein phosphorylation, Molecular Weight, chemistry, protein kinase B, cell function, I kappa B alpha, Proto-Oncogene Proteins c-akt
Abstract

Several studies indicate that hyaluronan oligosaccharides (oHA) are able to modulate growth and cell survival in solid tumors; however, no studies have been undertaken to analyze the effect of oHA on T-lymphoid disorders. In this work we showed that oHA were able to induce apoptosis in lymphoma cell lines. Since PI3-K/Akt and nuclear factor-κB (NF-κB) are major factors involved in cell survival and anti-apoptotic pathways in lymphoma cells, we hypothesized that oHA could induce apoptosis through inhibition of these pathways. oHA were identified by a method which allows characterization of length using a high pH anion exchange chromatography with pulse amperometric detection (HPAEC-PAD). oHA inhibited PIP3 production (principal product of PI3-K activity) and reduced Akt phosphorylation levels, similarly to the specific inhibitor wortmannin. However, treatment with either oHA or wortmannin failed to inhibit constitutive NF-κB activity and modulate IκBα protein levels, suggesting that PI3-K and NF-κB signaling pathways are not related in the cell lines used. Cell behavior differed using native hyaluronan (HA), which induced PIP3 production, Akt phosphorylation, and NF-κB activation, although not related with cell survival since treatment with native HA showed no effect on apoptosis. Our results suggest that oHA induce apoptosis by suppression of PI3-K/Akt cell survival pathway without involving NF-κB activation, through a mechanism that differs from the one mediated by native HA. © 2006 Oxford University Press. Fil:Gallo-Rodriguez, C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Agusti, R. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.

Published
2006

3. Hyaluronan oligosaccharides induce cell death through PI3-K/Akt pathway independently of NF-κB transcription factor.

Author

Laura Alaniz, Mariana G. García, Carola Gallo-Rodriguez, Rosalía Agusti, and Norma Sterín-Speziale

Abstract

Several studies indicate that hyaluronan oligosaccharides (oHA) are able to modulate growth and cell survival in solid tumors; however, no studies have been undertaken to analyze the effect of oHA on T-lymphoid disorders. In this work we showed that oHA were able to induce apoptosis in lymphoma cell lines. Since PI3-K/Akt and nuclear factor-κB (NF-κB) are major factors involved in cell survival and anti-apoptotic pathways in lymphoma cells, we hypothesized that oHA could induce apoptosis through inhibition of these pathways. oHA were identified by a method which allows characterization of length using a high pH anion exchange chromatography with pulse amperometric detection (HPAEC-PAD). oHA inhibited PIP3 production (principal product of PI3-K activity) and reduced Akt phosphorylation levels, similarly to the specific inhibitor wortmannin. However, treatment with either oHA or wortmannin failed to inhibit constitutive NF-κB activity and modulate IκBα protein levels, suggesting that PI3-K and NF-κB signaling pathways are not related in the cell lines used. Cell behavior differed using native hyaluronan (HA), which induced PIP3 production, Akt phosphorylation, and NF-κB activation, although not related with cell survival since treatment with native HA showed no effect on apoptosis. Our results suggest that oHA induce apoptosis by suppression of PI3-K/Akt cell survival pathway without involving NF-κB activation, through a mechanism that differs from the one mediated by native HA. [ABSTRACT FROM AUTHOR]

Published
2006
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