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51. FAM49B, a novel regulator of mitochondrial function and integrity that suppresses tumor metastasis

Author

Chattaragada, M S, primary, Riganti, C, additional, Sassoe, M, additional, Principe, M, additional, Santamorena, M M, additional, Roux, C, additional, Curcio, C, additional, Evangelista, A, additional, Allavena, P, additional, Salvia, R, additional, Rusev, B, additional, Scarpa, A, additional, Cappello, P, additional, and Novelli, F, additional

Published
2017
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56. Mitochondria-targeted doxorubicin: A new therapeutic strategy against drug-resistant osteosarcoma

Author

Buondonno, I., primary, Gazzano, E., additional, Sea Rin, J., additional, Audrito, V., additional, Kopecka, J., additional, Fanelli, M., additional, Salaroglio, I.C., additional, Costamagna, C., additional, Roato, I., additional, Mungo, E., additional, Hattinger, C., additional, Deaglio, S., additional, Kelley, S., additional, Serra, M., additional, and Riganti, C., additional

Published
2016
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58. Safety and Efficacy of Magnet Use to Temporarily Inhibit Inappropriate Subcutaneous Implantable Cardioverter Defibrillator Therapy in Emergency Situations: A Case Report

Author

Santomauro Maurizio, Riganti Carla, Santomauro Mario Alberto, Viggiano Aniello, Castellano Gaetano, Iovino Gianluigi, Rapacciuolo Antonio, Fiore Francesco, Cacciatore Francesco, and Esposito Giovanni

Subjects
subcutaneous implantable cardioverter defibrillator, inappropriate shock, clinical magnet, inhibition shock therapy, magnet interference, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Introduction: The subcutaneous implantable cardioverter defibrillator (S-ICD) represents a major advancement in ICD technology. Inappropriate shocks (IAS) occur in more than 3.1% of the population with S-ICD each year and are usually followed by admission to the emergency department (ED). In this setting, the disabling of IAS is mandatory during a pseudo-electrical storm (ES). This report describes the strategies that can be followed in order to temporarily inhibit IAS in critical care settings with the use of magnets.

Published
2022
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65. Sicurezza e privacy

Author

TRIASSI, MARIA, RIGANTI C, SCAFARTO MV, QUAGLIATA L, NEGRONE M., Triassi, Maria, Riganti, C, Scafarto, Mv, Quagliata, L, and Negrone, M.

Published
2005

71. The association of statins plus LDL receptor-targeted liposome-encapsulated doxorubicin increases the in vitro drug delivery across blood-brain barrier cells

Author

Pinzón?Daza, ML, Couraud, PO, Romero, IA, Weksler, B, Ghigo, D, Bosia, A, Riganti, C, and Garzón, Ruth

Subjects
Simvastatin, Unclassified drug, Nanoparticle, Compactin, Receptors, Blood-brain barrier, P-glycoprotein, statins, nitric oxide, doxorubicin, liposomal drugs, low density lipoprotein, Rho kinase, Enzyme activity, Low-density lipoproteins receptor, Drug dosage form comparison, Priority journal, rho-Associated Kinases, NF-kappa B, Drug transport, Breast cancer resistance protein, Research Papers, Blood brain barrier, Liposomal delivery, Microvascular endothelial cell, Drug mechanism, Human, Drug cytotoxicity, tumor, Low density lipoprotein receptor, Drug potentiation, Atp-binding cassette transporters, Rho-associated kinases, Article, Cell Line, Hydroxymethylglutaryl-coa reductase inhibitors, Cell Line, Tumor, Rhoa kinase, Humans, Lovastatin, Nitrites, Central nervous system tumours, Nitric oxide synthase, Drug receptor binding, Statins, In vitro study, Multidrug resistance protein, Nitric oxide, Tumor cell line, ldl, Drug efficacy, Immunoglobulin enhancer binding protein, Human cell, Receptors, LDL, Doxorubicin, Nf-kappa b, Drug penetration, Rhoa gtp-binding protein, Liposomes, Protein expression, ATP-Binding Cassette Transporters, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Nitric Oxide Synthase, Glioblastoma, Cell line, rhoA GTP-Binding Protein, Rhoa guanine nucleotide binding protein, Controlled study, Brain cell
Abstract

Background and PurposeThe passage of drugs across the blood-brain barrier (BBB) limits the efficacy of chemotherapy in brain tumours. For instance, the anticancer drug doxorubicin, which is effective against glioblastoma in vitro, has poor efficacy in vivo, because it is extruded by P-glycoprotein (Pgp/ABCB1), multidrug resistance-related proteins and breast cancer resistance protein (BCRP/ABCG2) in BBB cells. The aim of this study was to convert poorly permeant drugs like doxorubicin into drugs able to cross the BBB. Experimental ApproachExperiments were performed on primary human cerebral microvascular endothelial hCMEC/D3 cells, alone and co-cultured with human brain and epithelial tumour cells. Key ResultsStatins reduced the efflux activity of Pgp/ABCB1 and BCRP/ABCG2 in hCMEC/D3 cells by increasing the synthesis of NO, which elicits the nitration of critical tyrosine residues on these transporters. Statins also increased the number of low-density lipoprotein (LDL) receptors exposed on the surface of BBB cells, as well as on tumour cells like human glioblastoma. We showed that the association of statins plus drug-loaded nanoparticles engineered as LDLs was effective as a vehicle for non-permeant drugs like doxorubicin to cross the BBB, allowing its delivery into primary and metastatic brain tumour cells and to achieve significant anti-tumour cytotoxicity. Conclusions and ImplicationsWe suggest that our 'Trojan horse' approach, based on the administration of statins plus a LDL receptor-targeted liposomal drug, might have potential applications in the pharmacological therapy of different brain diseases for which the BBB represents an obstacle. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

Published
2012

72. Experimental glioblastoma in the fisher rat model: Treatment with a biocompatible system as carrier of methotrexate

Author

Biasibetti, E., primary, Valazza, A., additional, Battaglia, L., additional, Gallarate, M., additional, Peira, E., additional, Chirio, D., additional, Muntoni, E., additional, Panciani, P.P., additional, Riganti, C., additional, Annovazzi, L., additional, Caldera, V., additional, Schiffer, D., additional, Lanotte, M., additional, and Capucchio, M.T., additional

Published
2015
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75. Solid Lipid Nanoparticles as Antineoplastic Drug Vehicles in Glioblastoma Multiforme: In-vitro and In-vivo Pathological Effects

Author

Biasibetti, E., primary, Battaglia, L., additional, Gallarate, M., additional, Peira, E., additional, Chirio, D., additional, Muntoni, E., additional, Valazza, A., additional, Lanotte, M., additional, Panciani, P.P., additional, Riganti, C., additional, Annovazzi, L., additional, Caldera, V., additional, Schiffer, D., additional, and Capucchio, M.T., additional

Published
2014
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79. FAM49B, a novel regulator of mitochondrial function and integrity that suppresses tumor metastasis

Author

Chattaragada, M S, Riganti, C, Sassoe, M, Principe, M, Santamorena, M M, Roux, C, Curcio, C, Evangelista, A, Allavena, P, Salvia, R, Rusev, B, Scarpa, A, Cappello, P, and Novelli, F

Abstract

Mitochondrial dysregulation plays a central role in cancers and drives reactive oxygen species (ROS)-dependent tumor progression. We investigated the pro-tumoral roles of mitochondrial dynamics and altered intracellular ROS levels in pancreatic ductal adenocarcinoma (PDAC). We identified ‘family with sequence similarity 49 member B’ (FAM49B) as a mitochondria-localized protein that regulates mitochondrial fission and cancer progression. Silencing FAM49B in PDAC cells resulted in increased fission and mitochondrial ROS generation, which enhanced PDAC cell proliferation and invasion. Notably, FAM49B expression levels in PDAC cells were downregulated by the tumor microenvironment. Overall, the results of this study show that FAM49B acts as a suppressor of cancer cell proliferation and invasion in PDAC by regulating tumor mitochondrial redox reactions and metabolism.

Published
2018
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83. 2.37 Accelerated Activity of the Mevalonate Pathway Supports the Immune Escape and Multidrug- Resistance Phenotype of IGHV Unmutated Chronic Lymphocytic Leukemia Cells

Author

Coscia, M., primary, Rigoni, M., additional, Riganti, C., additional, Campia, I., additional, Vitale, C., additional, Griggio, V., additional, Peola, S., additional, Castella, B., additional, Pantaleoni, F., additional, Sciancalepore, P., additional, Drandi, D., additional, Omede, P., additional, Ladetto, M., additional, Bosia, A., additional, Boccadoro, M., additional, and Massaia, M., additional

Published
2011
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85. Fluoride Effects: The Two Faces of Janus

Author

Gazzano, E., primary, Bergandi, L., additional, Riganti, C., additional, Aldieri, E., additional, Doublier, S., additional, Costamagna, C., additional, Bosia, A., additional, and Ghigo, D., additional

Published
2010
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98. Nitric oxide reverts the resistance to doxorubicin in human colon cancer cells by inhibiting the drug efflux

Author

Bosia, A., Costamagna, C., Dario Ghigo, Miraglia, E., Pescarmona, G., Riganti, C., and Viarisio, D.

Subjects
Cancer Research, Antibiotics, Antineoplastic, Nitrates, doxorubicin, nitric oxide, multidrug resistance, P-glycoprotein, MDR-associated proteins, S-Nitroso-N-Acetylpenicillamine, Drug Resistance, Multiple, Isoenzymes, Oncology, Drug Resistance, Neoplasm, Colonic Neoplasms, Humans, Multidrug Resistance-Associated Proteins, Nitric Oxide Synthase, Cyclic GMP, HT29 Cells
Abstract

Multidrug resistance (MDR) is a phenomenon by which cancer cells evade the cytotoxic effects of chemotherapeutic agents. It may occur through different mechanisms, but it often correlates with the overexpression of integral membrane transporters, such as P-glycoprotein (Pgp) and MDR-associated proteins (MRPs), with resulting decrease of drug accumulation and cellular death. Doxorubicin is a substrate of Pgp; it has been suggested that its ability to induce synthesis of nitric oxide (NO) could explain, at least in part, its cytotoxic effects. Culturing the human epithelial colon cell line HT29 in the presence of doxorubicin, we obtained a doxorubicin-resistant (HT29-dx) cell population: these cells accumulated less intracellular doxorubicin, were less sensitive to the cytotoxic effects of doxorubicin and cisplatin, overexpressed Pgp and MRP3, and exhibited a lower NO production (both under basal conditions and after doxorubicin stimulation). The resistance to doxorubicin could be reversed when HT29-dx cells were incubated with inducers of NO synthesis (cytokines mix, atorvastatin). Some NO donors increased the drug accumulation in HT29-dx cells in a guarosine-3′:5′-cyclic monophosphate–independent way; this effect was associated with a marked reduction of doxorubicin efflux rate in HT29 and HT29-dx cells, and tyrosine nitration in the MRP3 protein. Our results suggest that onset of MDR and impairment of NO synthesis are related; this finding could point to a new strategy to reverse doxorubicin resistance in human cancer.

99. HIF-1 activation induces doxorubicin resistance in MCF7 3-D spheroids via P-glycoprotein expression: a potential model of the chemo-resistance of invasive micropapillary carcinoma of the breast

Author

Doublier Sophie, Belisario Dimas C, Polimeni Manuela, Annaratone Laura, Riganti Chiara, Allia Elena, Ghigo Dario, Bosia Amalia, and Sapino Anna

Subjects
HIF-1α, 3-D spheroids, Elastase, Invasive micropapillary breast carcinoma, Doxorubicin resistance, P-glycoprotein, MUC-1, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Invasive micropapillary carcinoma (IMPC) of the breast is a distinct and aggressive variant of luminal type B breast cancer that does not respond to neoadjuvant chemotherapy. It is characterized by small pseudopapillary clusters of cancer cells with inverted cell polarity. To investigate whether hypoxia-inducible factor-1 (HIF-1) activation may be related to the drug resistance described in this tumor, we used MCF7 cancer cells cultured as 3-D spheroids, which morphologically simulate IMPC cell clusters. Methods HIF-1 activation was measured by EMSA and ELISA in MCF7 3-D spheroids and MCF7 monolayers. Binding of HIF-1α to MDR-1 gene promoter and modulation of P-glycoprotein (Pgp) expression was evaluated by ChIP assay and FACS analysis, respectively. Intracellular doxorubicin retention was measured by spectrofluorimetric assay and drug cytotoxicity by annexin V-FITC measurement and caspase activity assay. Results In MCF7 3-D spheroids HIF-1 was activated and recruited to participate to the transcriptional activity of MDR-1 gene, coding for Pgp. In addition, Pgp expression on the surface of cells obtained from 3-D spheroids was increased. MCF7 3-D spheroids accumulate less doxorubicin and are less sensitive to its cytotoxic effects than MCF7 cells cultured as monolayer. Finally, HIF-1α inhibition either by incubating cells with 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (a widely used HIF-1α inhibitor) or by transfecting cells with specific siRNA for HIF-1α significantly decreased the expression of Pgp on the surface of cells and increased the intracellular doxorubicin accumulation in MCF7 3-D spheroids. Conclusions MCF7 breast cancer cells cultured as 3-D spheroids are resistant to doxorubicin and this resistance is associated with an increased Pgp expression in the plasma membrane via activation of HIF-1. The same mechanism may be suggested for IMPC drug resistance.

Published
2012
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100. iNOS activity is necessary for the cytotoxic and immunogenic effects of doxorubicin in human colon cancer cells

Author

Ghigo Dario, Matera Lina, Gazzano Elena, Brusa Davide, Kopecka Joanna, De Boo Sara, Bosia Amalia, and Riganti Chiara

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Doxorubicin is one of the few chemotherapeutic drugs able to exert both cytotoxic and pro-immunogenic effects against cancer cells. Following the drug administration, the intracellular protein calreticulin is translocated with an unknown mechanism onto the plasma membrane, where it triggers the phagocytosis of tumour cells by dendritic cells. Moreover doxorubicin up-regulates the inducible nitric oxide (NO) synthase (iNOS) gene in cancer cells, leading to huge amounts of NO, which in turn acts as a mediator of the drug toxicity and as a chemosensitizer agent in colon cancer. Indeed by nitrating tyrosine on the multidrug resistance related protein 3, NO decreases the doxorubicin efflux from tumour cells and enhances the drug toxicity. It is not clear if NO, beside playing a role in chemosensitivity, may also play a role in doxorubicin pro-immunogenic effects. To clarify this issue, we compared the doxorubicin-sensitive human colon cancer HT29 cells with the drug-resistant HT29-dx cells and the HT29 cells silenced for iNOS (HT29 iNOS-). Results In both HT29-dx and HT29 iNOS- cells, doxorubicin did not induce NO synthesis, had a lower intracellular accumulation and a lower toxicity. Moreover the drug failed to promote the translocation of calreticulin and the phagocytosis of HT29-dx and HT29 iNOS-cells, which resulted both chemoresistant and immunoresistant. However, if NO levels were exogenously increased by sodium nitroprusside, the chemosensitivity to doxorubicin was restored in HT29 iNOS-cells. In parallel the NO donor per se was sufficient to induce the exposure of calreticulin and to increase the phagocytosis of HT29 iNOS- cells by DCs and their functional maturation, thus mimicking the pro-immunogenic effects exerted by doxorubicin in the parental drug-sensitive HT29 cells. Conclusion Our data suggest that chemo- and immuno-resistance to anthracyclines are associated in colon cancer cells and rely on a common mechanism, that is the inability of doxorubicin to induce iNOS. Therefore NO donors might represent a promising strategy to restore both chemosensitivity and immunosensitivity to doxorubicin in resistant cells.

Published
2009
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