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dc.provenanceCONICET-
dc.creatorCirigliano, Stéfano Martín-
dc.creatorDíaz Bessone, María Inés-
dc.creatorBerardi, Damian Emilio-
dc.creatorFlumian, Carolina-
dc.creatorBal, Elisa Dora-
dc.creatorPerea, Silvio E.-
dc.creatorFarina, Hernán Gabriel-
dc.creatorTodaro, Laura Beatriz-
dc.creatorUrtreger, Alejandro Jorge-
dc.date2018-07-10T16:59:04Z-
dc.date2018-07-10T16:59:04Z-
dc.date2017-03-
dc.date2018-06-07T14:11:02Z-
dc.date.accessioned2019-04-29T15:32:53Z-
dc.date.available2019-04-29T15:32:53Z-
dc.date.issued2018-07-10T16:59:04Z-
dc.date.issued2018-07-10T16:59:04Z-
dc.date.issued2017-03-
dc.date.issued2018-06-07T14:11:02Z-
dc.identifierCirigliano, Stéfano Martín; Díaz Bessone, María Inés; Berardi, Damian Emilio; Flumian, Carolina; Bal, Elisa Dora; et al.; The synthetic peptide CIGB-300 modulates CK2-dependent signaling pathways affecting the survival and chemoresistance of non-small cell lung cancer cell lines; BioMed Central; Cancer Cell International; 17; 1; 3-2017; 1-16-
dc.identifier1475-2867-
dc.identifierhttp://hdl.handle.net/11336/51603-
dc.identifierCONICET Digital-
dc.identifierCONICET-
dc.identifier.urihttp://rodna.bn.gov.ar:8080/jspui/handle/bnmm/296259-
dc.descriptionBackground: Lung cancer is the most frequently diagnosed cancer and the leading cause of cancer-related deaths worldwide. Up to 80% of cancer patients are classified as non-small-cell lung cancer (NSCLC) and cisplatin remains as the gold standard chemotherapy treatment, despite its limited efficacy due to both intrinsic and acquired resistance. The CK2 is a Ser/Thr kinase overexpressed in various types of cancer, including lung cancer. CIGB-300 is an antitumor peptide with a novel mechanism of action, since it binds to CK2 substrates thus preventing the enzyme activity. The aim of this work was to analyze the effects of CIGB-300 treatment targeting CK2-dependent signaling pathways in NSCLC cell lines and whether it may help improve current chemotherapy treatment. Methods: The human NSCLC cell lines NCI-H125 and NIH-A549 were used. Tumor spheroids were obtained through the hanging-drop method. A cisplatin resistant A549 cell line was obtained by chronic administration of cisplatin. Cell viability, apoptosis, immunoblotting, immunofluorescence and luciferase reporter assays were used to assess CIGB-300 effects. A luminescent assay was used to monitor proteasome activity. Results: We demonstrated that CIGB-300 induces an anti-proliferative response both in monolayer- and three-dimensional NSCLC models, presenting rapid and complete peptide uptake. This effect was accompanied by the inhibition of the CK2-dependent canonical NF-ΚB pathway, evidenced by reduced RelA/p65 nuclear levels and NF-ΚB protein targets modulation in both lung cancer cell lines, as well as conditionally reduced NF-ΚB transcriptional activity. In addition, NF-ΚB modulation was associated with enhanced proteasome activity, possibly through its α7/C8 subunit. Neither the peptide nor a classical CK2 inhibitor affected cytoplasmic β-CATENIN basal levels. Given that NF-ΚB activation has been linked to cisplatin-induced resistance, we explored whether CIGB-300 could bring additional therapeutic benefits to the standard cisplatin treatment. We established a resistant cell line that showed higher p65 nuclear levels after cisplatin treatment as compared with the parental cell line. Remarkably, the cisplatin-resistant cell line became more sensitive to CIGB-300 treatment. Conclusions: Our data provide new insights into CIGB-300 mechanism of action and suggest clinical potential on current NSCLC therapy.-
dc.descriptionFil: Cirigliano, Stéfano Martín. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina-
dc.descriptionFil: Díaz Bessone, María Inés. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina-
dc.descriptionFil: Berardi, Damian Emilio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina-
dc.descriptionFil: Flumian, Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina-
dc.descriptionFil: Bal, Elisa Dora. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina-
dc.descriptionFil: Perea, Silvio E.. Centro de Genética Ingeniería y Biotecnología; Cuba-
dc.descriptionFil: Farina, Hernán Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología. Laboratorio de Oncología Molecular; Argentina-
dc.descriptionFil: Todaro, Laura Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina-
dc.descriptionFil: Urtreger, Alejandro Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherBioMed Central-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1186/s12935-017-0413-y-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://cancerci.biomedcentral.com/articles/10.1186/s12935-017-0413-y-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttps://creativecommons.org/licenses/by/2.5/ar/-
dc.sourcereponame:CONICET Digital (CONICET)-
dc.sourceinstname:Consejo Nacional de Investigaciones Científicas y Técnicas-
dc.sourceinstacron:CONICET-
dc.source.urihttp://hdl.handle.net/11336/51603-
dc.subjectCIGB-300-
dc.subjectCK2-
dc.subjectNF-ΚB-
dc.subjectNSCLC-
dc.subjectInmunología-
dc.subjectMedicina Básica-
dc.subjectCIENCIAS MÉDICAS Y DE LA SALUD-
dc.titleThe synthetic peptide CIGB-300 modulates CK2-dependent signaling pathways affecting the survival and chemoresistance of non-small cell lung cancer cell lines-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.typeinfo:ar-repo/semantics/articulo-
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