dc.creator | Parra, Eduardo | |
dc.creator | Ferreira Parker, Jorge | |
dc.creator | Gutiérrez, Luis | |
dc.date.accessioned | 2019-01-29T13:56:13Z | |
dc.date.available | 2019-01-29T13:56:13Z | |
dc.date.created | 2019-01-29T13:56:13Z | |
dc.date.issued | 2014 | |
dc.identifier | Oncology Reports 31: 422-427, 2014 | |
dc.identifier | 1021335X | |
dc.identifier | 17912431 | |
dc.identifier | 10.3892/or.2013.2829 | |
dc.identifier | https://repositorio.uchile.cl/handle/2250/160097 | |
dc.description.abstract | Early growth response-1 (Egr-1) and the non-receptor protein tyrosine kinase (c-Abl) are 2 response genes that can act as regulators of cell growth and apoptosis in response to stress. Both Egr-1 and c-Abl regulate cell proliferation and survival in different types of cancer cells. To study the effect of overexpression of EGR-1 on the activity of c-Abl in prostate cancer cells, human PC-3 and LNCaP cells were transfected with a control vector or a vector containing the murine Egr-1 cDNA and assessed for the expression of the c-Abl gene. Cells overexpressing Egr-1 were studied with respect to apoptosis (Annexin V)/DEVDase activity, Egr-1/c-Abl activation (western blotting) and cell proliferation (MTT assay). The cells were exposed to tumor necrosis factor (TNF-), a known inductor of Egr-1, to c-Abl inhibitor STI-571 and to small interfering RNA (siRNA)-Egr-1, respectively. The results from our studies strongly suggest that overexpression of Egr-1 decreased c-Abl activity independent of endogenous Egr-1 inhibition by siRNA-Egr-1. | |
dc.language | en | |
dc.publisher | Spandidos Publ | |
dc.rights | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | |
dc.rights | Attribution-NonCommercial-NoDerivs 3.0 Chile | |
dc.source | Oncology Reports | |
dc.subject | Apoptosis | |
dc.subject | c-Abl | |
dc.subject | Early growth response-1 | |
dc.subject | PC-3/LNCaP | |
dc.title | Decreased c-Abl activity in PC-3 and LNCaP prostate cancer cells overexpressing the early growth response-1 protein | |
dc.type | Artículo de revista | |