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Your search keyword '"Spatuzza, Michela"' showing total 3 results
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3 results on '"Spatuzza, Michela"'

1. Effect of Ferulic Acid Loaded in Nanoparticle on Tissue Transglutaminase Expression Levels in Human Glioblastoma Cell Line.

Author

Dell'Albani, Paola, Carbone, Claudia, Sposito, Giovanni, Spatuzza, Michela, Chiacchio, Maria Assunta, Grasso, Rosaria, Legnani, Laura, Santonocito, Debora, Puglia, Carmelo, Parenti, Rosalba, Puglisi, Giovanni, and Campisi, Agatina

Subjects
FERULIC acid, CELL cycle, GLIOBLASTOMA multiforme, GLIOMAS, CELL lines
Abstract

Glioblastoma (GBM) is one of the most aggressive cancers, characterized by a decrease in antioxidant levels. Evidence has demonstrated that ferulic acid (FA), a natural antioxidant particularly abundant in vegetables and fruits, could be a promising candidate for GBM treatment. Since FA shows a high instability that compromises its therapeutic application, it has been encapsulated into Nanostructured Lipid Carriers (NLCs) to improve its bioavailability in the brain. It has been demonstrated that tissue transglutaminase (TG2) is a multi-functional protein implicated in many physiological and pathological processes, including cancer. TG2 is also involved in GBM correlated with metastasis formation and drug resistance. Therefore, the evaluation of TG2 expression levels and its cellular localization are important to assess the anti-cancer effect of FA against GBM cancer. Our results have demonstrated that treatment with free FA and FA-NLCs in the U87-MG cancer cell line differently modified TG2 localization and expression levels. In the cells treated with free FA, TG2 appeared expressed both in the cytosol and in the nucleus, while the treatment with FA-NLCs showed that the protein is exclusively localized in the cytosol, exerting its pro-apoptotic effect. Therefore, our data suggest that FA loaded in NLCs could represent a promising natural agent for supplementing the current anti-cancer drugs used for the treatment of GBM. [ABSTRACT FROM AUTHOR]

Published
2024
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2. Novel cross talk between IGF-IR and DDR1 regulates IGF-IR trafficking, signaling and biological responses

Author

Malaguarnera, Roberta, Nicolosi, Maria Luisa, Sacco, Antonella, Morcavallo, Alaide, Vella, Veronica, Voci, Concetta, Spatuzza, Michela, Shi-Qiong, Xu, Iozzo, Renato V., Vigneri, Riccardo, Morrione, Andrea, and Belfiore, Antonino

Subjects
Breast cancer, DDR1, IGF-IR, Insulin-like growth factor-I receptor, Animals, Apoptosis, Blotting, Western, Cell Cycle, Cell Movement, Cell Proliferation, Cells, Cultured, Discoidin Domain Receptor 1, Enzyme-Linked Immunosorbent Assay, Fibroblasts, Humans, Immunoprecipitation, Mice, Microscopy, Confocal, Neoplasms, Phosphorylation, Protein Transport, RNA, Messenger, RNA, Small Interfering, Real-Time Polymerase Chain Reaction, Receptor Protein-Tyrosine Kinases, Receptors, Somatomedin, Reverse Transcriptase Polymerase Chain Reaction, Tyrosine, Oncology, Messenger, Somatomedin, Tumor initiation, Receptor, IGF Type 1, Prostate cancer, 0302 clinical medicine, Receptors, Receptor, 0303 health sciences, Microscopy, Cultured, Blotting, Cell cycle, 3. Good health, 030220 oncology & carcinogenesis, Confocal, Western, Research Paper, Cells, insulin-like growth factor-I receptor, Biology, Small Interfering, 03 medical and health sciences, breast cancer, medicine, 030304 developmental biology, Cancer, medicine.disease, Cancer cell, Cancer research, RNA
Abstract

// Roberta Malaguarnera 1, * , Maria Luisa Nicolosi 1, * , Antonella Sacco 1 , Alaide Morcavallo 1 , Veronica Vella 2 , Concetta Voci 1 , Michela Spatuzza 3 , Shi-Qiong Xu 4 , Renato V. Iozzo 5 , Riccardo Vigneri 6 , Andrea Morrione 4 , Antonino Belfiore 1 1 Endocrinology, Department of Health Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy 2 Motor Sciences, School of Human and Social Sciences, Kore University of Enna, Enna, Italy 3 Institute of Neurological Sciences, National Research Council, Catania, Italy 4 Department of Urology and Biology of Prostate Cancer Program, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA 5 Department of Pathology, Anatomy and Cell Biology and Cancer Cell Biology and Signaling Program, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA 6 Endocrinology, Department of Clinical and Sperimental Medicine, University of Catania, Garibaldi-Nesima Hospital, Catania, Italy * These authors have contributed equally to this work Correspondence to: Antonino Belfiore, e-mail: belfiore@unicz.it Andrea Morrione, e-mail: andrea.morrione@jefferson.edu Keywords: IGF-IR, insulin-like growth factor-I receptor, DDR1, breast cancer Received: September 01, 2014 Accepted: January 25, 2015 Published: March 28, 2015 ABSTRACT The insulin-like growth factor-I receptor (IGF-IR), plays a key role in regulating mammalian development and growth, and is frequently deregulated in cancer contributing to tumor initiation and progression. Discoidin domain receptor 1 (DDR1), a collagen receptor tyrosine-kinase, is as well frequently overexpressed in cancer and implicated in cancer progression. Thus, we investigated whether a functional cross-talk between the IGF-IR and DDR1 exists and plays any role in cancer progression. Using human breast cancer cells we found that DDR1 constitutively associated with the IGF-IR. However, this interaction was enhanced by IGF-I stimulation, which promoted rapid DDR1 tyrosine-phosphorylation and co-internalization with the IGF-IR. Significantly, DDR1 was critical for IGF-IR endocytosis and trafficking into early endosomes, IGF-IR protein expression and IGF-I intracellular signaling and biological effects, including cell proliferation, migration and colony formation. These biological responses were inhibited by DDR1 silencing and enhanced by DDR1 overexpression. Experiments in mouse fibroblasts co-transfected with the human IGF-IR and DDR1 gave similar results and indicated that, in the absence of IGF-IR, collagen-dependent phosphorylation of DDR1 is impaired. These results demonstrate a critical role of DDR1 in the regulation of IGF-IR action, and identify DDR1 as a novel important target for breast cancers that overexpress IGF-IR.

Published
2014

3. The antineoplastic drug flavopiridol reverses memory impairment induced by Amyloid-ß1-42 oligomers in mice.

Author

Leggio, Gian Marco, Catania, Maria Vincenza, Puzzo, Daniela, Spatuzza, Michela, Pellitteri, Rosalia, Gulisano, Walter, Torrisi, Sebastiano Alfio, Giurdanella, Giovanni, Piazza, Cateno, Impellizzeri, Agata Rita, Gozzo, Lucia, Navarria, Andrea, Bucolo, Claudio, Nicoletti, Ferdinando, Palmeri, Agostino, Salomone, Salvatore, Copani, Agata, Caraci, Filippo, and Drago, Filippo

Subjects
*ANTINEOPLASTIC agents, *MEMORY disorders, *ANIMAL models of Alzheimer's disease, *CELL cycle regulation, *AMYLOID beta-protein, *CYCLIN-dependent kinase inhibitors, *DISEASE risk factors, ANIMAL models of memory disorders
Abstract

The ectopic re-activation of cell cycle in neurons is an early event in the pathogenesis of Alzheimer’s disease (AD), which could lead to synaptic failure and ensuing cognitive deficits before frank neuronal death. Cytostatic drugs that act as cyclin-dependent kinase (CDK) inhibitors have been poorly investigated in animal models of AD. In the present study, we examined the effects of flavopiridol, an inhibitor of CDKs currently used as antineoplastic drug, against cell cycle reactivation and memory loss induced by intracerebroventricular injection of Aß 1-42 oligomers in CD1 mice. Cycling neurons, scored as NeuN-positive cells expressing cyclin A, were found both in the frontal cortex and in the hippocampus of Aβ-injected mice, paralleling memory deficits. Starting from three days after Aβ injection, flavopiridol (0.5, 1 and 3 mg/kg) was intraperitoneally injected daily, for eleven days. Here we show that a treatment with flavopiridol (0.5 and 1 mg/kg) was able to rescue the loss of memory induced by Aβ 1-42, and to prevent the occurrence of ectopic cell-cycle events in the mouse frontal cortex and hippocampus. This is the first evidence that a cytostatic drug can prevent cognitive deficits in a non-transgenic animal model of AD. [ABSTRACT FROM AUTHOR]

Published
2016
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