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dc.contributor.authorBuchegger, Kurt
dc.contributor.authorSilva, Ramón
dc.contributor.authorLopez, Jaime
dc.contributor.authorIli, Carmen
dc.contributor.authorAraya, Juan Carlos
dc.contributor.authorLeal, Pamela
dc.contributor.authorBrebi, Priscilla
dc.contributor.authorRiquelme, Ismael
dc.contributor.authorRoa, Juan Carlos
dc.date.accessioned2022-03-31T20:28:31Z
dc.date.available2022-03-31T20:28:31Z
dc.date.issued2017-05
dc.identifier10.1016/j.prp.2017.01.025
dc.identifier.urihttps://hdl.handle.net/20.500.12728/9994
dc.description.abstractGallbladder cancer (GBC) is a highly fatal disease with poor prognosis and few therapeutic alternatives. Molecular profiling has revealed that the deregulation in the ERK/MAPK signaling pathway plays a crucial role in many disease and malignancies, including GBC. The aim of this study was to measure the expression of ERK1/2 and p-ERK1/2 in a population with high GBC-related mortality, such as the Chilean population, and characterize the protein expression of this ERK/MAPK pathway in seven GBC cell lines. Immunohistochemistry (IHC) for ERK1/2 and p-ERK1/2 was performed in 123 GBC tissues and 37 chronic cholecystitis (CC) tissues. In addition, protein expression analysis by western blot for ERK1/2, p-ERK1/2, EGFR, ERBB2 and ERBB3 were performed in seven GBC cell lines (GB-d1, G415, NOZ, OCUG-1, TGBC-1, TGBC-2 and TGBC-24). A higher ERK1/2 and p-ERK1/2 expression was found in GBC tissues compared to chronic cholecystitis (CC) tissues (P < 0.001). However, neither significant differences in overall survival nor significant associations with any of the clinicopathological features were found by comparing low and high expression of both ERK1/2 and p-ERK1/2. Western blot analysis of seven GBC cell lines showed that, in general, GB-d1, G415 and NOZ cells evidenced a strong expression of ERK1/2, p-ERK1/2, EGFR, ERBB2 and ERBB3. Therefore, ERK1/2 and p-ERK1/2 seem to be important in the development of GBC and GB-d1, G415 and NOZ cell lines may be used as experimental models for further in vitro and in vivo studies that help to decipher the role of MAPK/ERK pathway in gallbladder carcinogenesis.es_ES
dc.description.sponsorshipThis work was supported by the Chilean National Fund for Sci-entific and Technological Development (FONDECYT) [11150802 toP.B., 11150622 to C.G.I., 1130204 to JCR 1151008 to P.L.]; CON-ICYT FONDAP 15130011 (ACCDis) and Millennium Institute onImmunology and Immunotherapy N◦P09- 016-F to JCR; and theProduction Development Corporation (CORFO) [N◦12IDL2-18157,N◦09CN14-5960 to CEGIN].es_ES
dc.language.isoenes_ES
dc.publisherPathology – Research and Practicees_ES
dc.subjectERK/MAPK pathwayERK1/2Gallbladder cancerImmunohistochemistryes_ES
dc.titleThe ERK/MAPK pathway is overexpressed and activated in gallbladder canceres_ES
dc.typeArticlees_ES


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