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3 results on '"Rigoletto S"'

1. Overcoming melanoma resistance to vemurafenib by targeting CCL2-induced miR-34a, miR-100 and miR-125b

Author

Vergani, E, Di Guardo, L, Dugo, M, Rigoletto, S, Tragni, G, Ruggeri, R, Perrone, F, Tamborini, E, Gloghini, A, Arienti, F, Vergani, B, Deho, P, De Cecco, L, Vallacchi, V, Frati, P, Shahaj, E, Villa, A, Santinami, M, De Braud, F, Rivoltini, L, Rodolfo, M, Rodolfo, M., VERGANI, BARBARA, VILLA, ANTONELLO, Vergani, E, Di Guardo, L, Dugo, M, Rigoletto, S, Tragni, G, Ruggeri, R, Perrone, F, Tamborini, E, Gloghini, A, Arienti, F, Vergani, B, Deho, P, De Cecco, L, Vallacchi, V, Frati, P, Shahaj, E, Villa, A, Santinami, M, De Braud, F, Rivoltini, L, Rodolfo, M, Rodolfo, M., VERGANI, BARBARA, and VILLA, ANTONELLO

Abstract

In melanoma, the adaptative cell response to BRAF inhibitors includes altered patterns of cytokine production contributing to tumor progression and drug resistance. Among the factors produced by PLX4032-resistant melanoma cell lines, CCL2 was higher compared to the sensitive parental cell lines and increased upon drug treatment. CCL2 acted as an autocrine growth factor for melanoma cells, stimulating the proliferation and resistance to apoptosis. In patients, CCL2 is detected in melanoma cells in tumors and in plasma at levels that correlate with tumor burden and lactate dehydrogenase. Vemurafenib treatment increased the CCL2 levels in plasma, whereas the long-term clinical response was associated with low CCL2 levels. Increased CCL2 production was associated with miRNA deregulation in the resistant cells. miR-34a, miR-100 and miR-125b showed high expression in both resistant cells and in tumor biopsies that were obtained from treated patients, and they were involved in the control of cell proliferation and apoptosis. Inhibition of CCL2 and of the selected miRNAs restored both the cell apoptosis and the drug efficacy in resistant melanoma cells. Therefore, CCL2 and miRNAs are potential prognostic factors and attractive targets for counteracting treatment resistance in metastatic melanoma.

Published
2016

2. Overcoming melanoma resistance to vemurafenib by targeting CCL2-induced miR-34a, miR-100 and miR-125b

Author

Viviana Vallacchi, Flavio Arienti, Elena Tamborini, Monica Rodolfo, Paola Frati, Elisabetta Vergani, Paola Deho, Filippo de Braud, Licia Rivoltini, Loris De Cecco, Barbara Vergani, Federica Perrone, Mario Santinami, Roberta Ruggeri, Gabrina Tragni, Antonello Villa, Lorenza Di Guardo, Annunziata Gloghini, Matteo Dugo, Sara Rigoletto, Eriomina Shahaj, Vergani, E, Di Guardo, L, Dugo, M, Rigoletto, S, Tragni, G, Ruggeri, R, Perrone, F, Tamborini, E, Gloghini, A, Arienti, F, Vergani, B, Deho, P, De Cecco, L, Vallacchi, V, Frati, P, Shahaj, E, Villa, A, Santinami, M, De Braud, F, Rivoltini, L, and Rodolfo, M

Subjects
0301 basic medicine, Male, Indoles, medicine.medical_treatment, Drug resistance, Tumor Cells, Cultured, Medicine, Vemurafenib, Chemokine CCL2, Sulfonamides, Reverse Transcriptase Polymerase Chain Reaction, Melanoma, Middle Aged, Prognosis, Gene Expression Regulation, Neoplastic, Survival Rate, Cytokine, Oncology, miRNAs, Female, MiRNA, CCL2, medicine.drug, Research Paper, Adult, BRAF inhibitor, Blotting, Western, Real-Time Polymerase Chain Reaction, 03 medical and health sciences, microRNA, melanoma, Humans, RNA, Messenger, Aged, Neoplasm Staging, drug resistance, business.industry, Cell growth, Gene Expression Profiling, medicine.disease, MicroRNAs, 030104 developmental biology, Apoptosis, Tumor progression, Drug Resistance, Neoplasm, Case-Control Studies, Immunology, Cancer research, business
Abstract

In melanoma, the adaptative cell response to BRAF inhibitors includes altered patterns of cytokine production contributing to tumor progression and drug resistance. Among the factors produced by PLX4032-resistant melanoma cell lines, CCL2 was higher compared to the sensitive parental cell lines and increased upon drug treatment. CCL2 acted as an autocrine growth factor for melanoma cells, stimulating the proliferation and resistance to apoptosis. In patients, CCL2 is detected in melanoma cells in tumors and in plasma at levels that correlate with tumor burden and lactate dehydrogenase. Vemurafenib treatment increased the CCL2 levels in plasma, whereas the long-term clinical response was associated with low CCL2 levels. Increased CCL2 production was associated with miRNA deregulation in the resistant cells. miR-34a, miR-100 and miR-125b showed high expression in both resistant cells and in tumor biopsies that were obtained from treated patients, and they were involved in the control of cell proliferation and apoptosis. Inhibition of CCL2 and of the selected miRNAs restored both the cell apoptosis and the drug efficacy in resistant melanoma cells. Therefore, CCL2 and miRNAs are potential prognostic factors and attractive targets for counteracting treatment resistance in metastatic melanoma.

Published
2015

3. Overcoming melanoma resistance to vemurafenib by targeting CCL2-induced miR-34a, miR-100 and miR-125b.

Author

Vergani E, Di Guardo L, Dugo M, Rigoletto S, Tragni G, Ruggeri R, Perrone F, Tamborini E, Gloghini A, Arienti F, Vergani B, Deho P, De Cecco L, Vallacchi V, Frati P, Shahaj E, Villa A, Santinami M, De Braud F, Rivoltini L, and Rodolfo M

Subjects
Adult, Aged, Blotting, Western, Case-Control Studies, Chemokine CCL2 genetics, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Male, Melanoma drug therapy, Melanoma metabolism, Melanoma pathology, Middle Aged, Neoplasm Staging, Prognosis, RNA, Messenger genetics, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Survival Rate, Tumor Cells, Cultured, Vemurafenib, Chemokine CCL2 metabolism, Drug Resistance, Neoplasm genetics, Indoles pharmacology, Melanoma genetics, MicroRNAs genetics, Sulfonamides pharmacology
Abstract

In melanoma, the adaptative cell response to BRAF inhibitors includes altered patterns of cytokine production contributing to tumor progression and drug resistance. Among the factors produced by PLX4032-resistant melanoma cell lines, CCL2 was higher compared to the sensitive parental cell lines and increased upon drug treatment. CCL2 acted as an autocrine growth factor for melanoma cells, stimulating the proliferation and resistance to apoptosis. In patients, CCL2 is detected in melanoma cells in tumors and in plasma at levels that correlate with tumor burden and lactate dehydrogenase. Vemurafenib treatment increased the CCL2 levels in plasma, whereas the long-term clinical response was associated with low CCL2 levels.Increased CCL2 production was associated with miRNA deregulation in the resistant cells. miR-34a, miR-100 and miR-125b showed high expression in both resistant cells and in tumor biopsies that were obtained from treated patients, and they were involved in the control of cell proliferation and apoptosis. Inhibition of CCL2 and of the selected miRNAs restored both the cell apoptosis and the drug efficacy in resistant melanoma cells. Therefore, CCL2 and miRNAs are potential prognostic factors and attractive targets for counteracting treatment resistance in metastatic melanoma.

Published
2016
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