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13 results on '"Battistelli C"'

7. Caratterizzazione chimica e tossicologica delle emissioni da carburanti alternativi per il trasporto pubblico nelle aree urbane

Author

Turrio Baldassarri L. 1, Battistelli C. 1, Conti L. 1, Crebelli R. 1, De Berardis B. 1, Iamiceli A.L. 1, Gambino M. 2, and Iannaccone S. 2

Subjects
Gas Naturale, Biodiesel, complex mixtures, Emissioni
Abstract

The Istituto Superiore di Sanità (ISS, the National Institute of Health of Italy) and the Istituto dei Motori (IM) of the Consiglio Nazionale delle Ricerche (CNR, National Research Council) have carried out this study, jointly funded by the two institutes together with the Ministry of Environment. The chemical and toxicological characteristics of emissions from two urban bus engines were studied: a diesel engine fueled with both diesel oil and biodiesel blend and an equivalent spark-ignition one fuelled with compressed natural gas, operating in steady-state conditions. Regulated and unregulated pollutants, such as carcinogenic polycyclic aromatic hydrocarbons and nitrated derivatives, carbonyl compounds and light aromatic hydrocarbons were quantified. Mutagenicity of the emissions was evaluated by the Salmonella typhimurium/mammalian microsome assay. The effect of the fuels under study on the size distribution of particulate matter was also evaluated. The impact of diesel-powered transport on urban air quality, and the potential benefits for human health deriving from the use of natural gas for public transport, are discussed.

Published
2008

11. Promotion of proliferation and metastasis of hepatocellular carcinoma by LncRNA00673 based on the targeted-regulation of notch signaling pathway

Author

Magistri, P., Battistelli, C., Assirati, G., Mereu, F., Tarantino, G., Gian Piero Guerrini, Ballarin, R., and Di Benedetto, F.

Subjects
Male, Mice, Inbred BALB C, Carcinoma, Hepatocellular, Receptors, Notch, Liver Neoplasms, surgical research, Mice, Nude, Apoptosis, Transfection, HCC, notch, long non-coding RNAs, small non-coding RNAs, Gene Expression Regulation, Neoplastic, Mice, Cell Line, Tumor, Animals, Humans, RNA, Long Noncoding, Cell Proliferation, Signal Transduction
Abstract

To investigate the relative expression of long non-coding RNA 00673 (lncRNA 00673) in hepatocellular carcinoma (HCC) and HCC cells and study its regulation on the malignant phenotype of HCC cells PATIENTS AND METHODS: Samples of HCC and adjacent tissues from January 2013 to December 2015 were collected. The expression level of lncRNA00673 in HCC tissues and cells was detected by quantitative Real-time polymerase chain reaction (qRT-PCR) assays. lncRNA00673 specific interference sequences were transiently transfected into HCC cells and the effect of HCC cells on the biological behavior of HCC cells was examined by in vitro experiments ((3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT assay), flow cytometry, transwell, etc.). A tumor model of nude mice with HCC was established for the study of tumor growth condition of tumor-bearing mice after the interference with lncRNA00673 expression. Changes in expression levels of molecular markers on Notch signaling pathway after the interference with lncRNA00673 were detected by Western blot.lncRNA00673 was highly expressed in HCC tissues and cells. MTT results showed that interfering with lncRNA00673 inhibited cell proliferation. Flow cytometry results showed that HCC cell cycle was retarded in G1-G0 phase, thus promoting apoptosis after the interference with lncRNA00673. Western blot results showed that expression levels of molecular markers on Notch signaling pathway were changed after the interference with lncRNA00763.lncRNA00673 is highly expressed in HCC tissues and cells, and can promote the proliferation and metastasis of HCC by the regulation on Notch signaling pathway. lncRNA00673 may be a potential target for the treatment of HCC.

12. Novel quinoline compounds active in cancer cells through coupled DNA methyltransferase inhibition and degradation

Author

Clemens Zwergel, Marco Tripodi, Donatella Del Bufalo, Annalisa Romanelli, Daniela Trisciuoglio, Cecilia Battistelli, Lucia Altucci, Giulia Stazi, Paola B. Arimondo, Rossella Fioravanti, Teresa De Luca, Alexandra Paulo, Dany Pechalrieu, Sergio Valente, Raffaele Strippoli, Angela Nebbioso, Federica Sarno, Eduarda Mendes, Antonello Mai, Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome] (UNIROMA), Università degli studi della Campania 'Luigi Vanvitelli' = University of the Study of Campania Luigi Vanvitelli, Universidade de Lisboa = University of Lisbon (ULISBOA), Istituto Nazionale di Malattie Infettive 'Lazzaro Spallanzani' (INMI), Department of Molecular Medicine, Institut Pasteur, Fondation Cenci Bolognetti - Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome] (UNIROMA), Pharmacochimie de la Régulation Epigénétique du Cancer (ETaC), PIERRE FABRE-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Chimie biologique épigénétique - Epigenetic Chemical Biology (EpiCBio), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), IFO - Istituto Nazionale Tumori Regina Elena [Roma] (IRE), CNR Istituto di Biologia e Patologia Molecolari [Roma] (CNR | IBPM), National Research Council of Italy | Consiglio Nazionale delle Ricerche (CNR), This work was supported by PRIN 2016 (prot. 20152TE5PK) (L.A., A.M.), Ricerca Finalizzata 2013 PE-2013-02355271 (A.M.), the Italian Association for Cancer Research AIRC-19162 (A.M.), AIRC-17217 (L.A.) and AIRC-18560 (D.D.B.), NIH (n. R01GM114306) (A.M.), VALERE: Vanvitelli per la Ricerca Program (L.A.), FP7-BLUEPRINT (282510) (L.A., A.M.), the Campania Regional Government Lotta alle Patologie Oncologiche (L.A.), iCURE (CUP B21c17000030007) (L.A.), Campania Regional Government FASE 2: IDEAL (CUP B63D18000560007) (L.A.), PlanCancer2014 (P.B.A.) and FCT, Portugal through UID/DTP/04138/2019 (A.P., E.M.) funds., Zwergel, C., Fioravanti, R., Stazi, G., Sarno, F., Battistelli, C., Romanelli, A., Nebbioso, A., Mendes, E., Paulo, A., Strippoli, R., Tripodi, M., Pechalrieu, D., Arimondo, P. B., De Luca, T., Del Bufalo, D., Trisciuoglio, D., Altucci, L., Valente, S., Mai, A., Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome], Università degli studi della Campania 'Luigi Vanvitelli', Universidade de Lisboa (ULISBOA), Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome]-Institut Pasteur, Fondation Cenci Bolognetti - Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Institute of Molecular Pathology and Biology [Rome] (IPBM), and Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome]-Consiglio Nazionale delle Ricerche (CNR)

Subjects
0301 basic medicine, Cancer Research, Methyltransferase, [SDV]Life Sciences [q-bio], Azacitidine, Decitabine, DNA methyltransferase, Apoptosis, Medicinal chemistry, Protein degradation, lcsh:RC254-282, Article, 03 medical and health sciences, 0302 clinical medicine, medicine, [CHIM]Chemical Sciences, Chemistry, Drug discovery, Apoptosi, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, 3. Good health, Enzyme inhibition, 030104 developmental biology, Oncology, Cell culture, 030220 oncology & carcinogenesis, Cancer cell, Cancer research, DNMT1, medicine.drug
Abstract

DNA methyltransferases (DNMTs) play a relevant role in epigenetic control of cancer cell survival and proliferation. Since only two DNMT inhibitors (azacitidine and decitabine) have been approved to date for the treatment of hematological malignancies, the development of novel potent and specific inhibitors is urgent. Here we describe the design, synthesis, and biological evaluation of a new series of compounds acting at the same time as DNMTs (mainly DNMT3A) inhibitors and degraders. Tested against leukemic and solid cancer cell lines, 2a&ndash, c and 4a&ndash, c (the last only for leukemias) displayed up to submicromolar antiproliferative activities. In HCT116 cells, such compounds induced EGFP gene expression in a promoter demethylation assay, confirming their demethylating activity in cells. In the same cell line, 2b and 4c chosen as representative samples induced DNMT1 and -3A protein degradation, suggesting for these compounds a double mechanism of DNMT3A inhibition and DNMT protein degradation.

Published
2020
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13. Spike-in SILAC proteomic approach reveals the vitronectin as an early molecular signature of liver fibrosis in hepatitis C infections with hepatic iron overload

Author

Leopoldo Paolo Pucillo, Andrea Baiocchini, Carmine Mancone, Franca Del Nonno, Marco Tripodi, Vera van Noort, Tonino Alonzi, Claudia Montaldo, Nicolina Rotiroti, Giuseppe Ippolito, Laura Amicone, Alice Conigliaro, Angela Maria Cozzolino, Cecilia Battistelli, Simone Mattei, Montaldo, C., Mattei, S., Baiocchini, A., Rotiroti, N., Nonno, F., Pucillo, L., Cozzolino, A., Battistelli, C., Amicone, L., Ippolito, G., van Noort, V., Conigliaro, A., Alonzi, T., Tripodi, M., Mancone, C., Department of Cellular Biotechnologies and Haematology, Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome]-Institut Pasteur, Fondation Cenci Bolognetti - Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), L. Spallanzani, National Institute for Infectious Diseases (IRCCS), European Molecular Biology Laboratory [Heidelberg] (EMBL), and This work was supported by grants from MIUR Ministero dell’Universit `a e Ricerca Scientifica (FIRB 2012, codice progetto RBFR12NSCF), Associazione Italiana per la Ricerca sul Cancro (AIRC) andMinistero della Salute (Ricerca Finalizzata 40H27, Ricerca Corrente).

Subjects
Liver Cirrhosis, Proteomics, hepatitis C virus, Male, MESH: Isotope Labeling, HSC, medicine.disease_cause, Biochemistry, 0302 clinical medicine, Fibrosis, MESH: Up-Regulation, Membrane Protein, hepatic stellate cell, liver fibrosis, hepatic iron overload, 0303 health sciences, biology, MESH: Proteomics, Medicine (all), hepatocellular carcinoma, Biomedicine, hepatitis c infection, vitronectin, Hepatitis C, [SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM], Up-Regulation, 3. Good health, cell culture-derived HCV, Isotope Labeling, 030220 oncology & carcinogenesis, Hepatocellular carcinoma, Hepatic iron overload, Hepatitis C infection, Liver fibrosis, Vitronectin, Biomarkers, Cell Line, Humans, Iron Overload, Membrane Proteins, Molecular Biology, HCV, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, Biomarker (medicine), MESH: Membrane Proteins, MESH: Liver Cirrhosis, Human, Liver Cirrhosi, Hepatitis C virus, MESH: Iron Overload, 03 medical and health sciences, medicine, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, 030304 developmental biology, MESH: Hepatitis C, MESH: Humans, MESH: Biological Markers, Liver fibrosi, Proteomic, Biomarker, medicine.disease, MESH: Vitronectin, MESH: Male, digestive system diseases, MESH: Cell Line, Biomedicine / Abbreviations: HCC, HCVcc, Immunology, Cancer research, Hepatic stellate cell, biology.protein, Steatosis
Abstract

Hepatitis C virus (HCV)-induced iron overload has been shown to promote liver fibrosis, steatosis, and hepatocellular carcinoma. The zonal-restricted histological distribution of pathological iron deposits has hampered the attempt to perform large-scale in vivo molecular investigations on the comorbidity between iron and HCV. Diagnostic and prognostic markers are not yet available to assess iron overload-induced liver fibrogenesis and progression in HCV infections. Here, by means of Spike-in SILAC proteomic approach, we first unveiled a specific membrane protein expression signature of HCV cell cultures in the presence of iron overload. Computational analysis of proteomic dataset highlighted the hepatocytic vitronectin expression as the most promising specific biomarker for iron-associated fibrogenesis in HCV infections. Next, the robustness of our in vitro findings was challenged in human liver biopsies by immunohistochemistry and yielded two major results: (i) hepatocytic vitronectin expression is associated to liver fibrogenesis in HCV-infected patients with iron overload; (ii) hepatic vitronectin expression was found to discriminate also the transition between mild to moderate fibrosis in HCV-infected patients without iron overload. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Published
2014

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