Decreased c-Abl activity in PC-3 and LNCaP prostate cancer cells overexpressing the early growth response-1 protein
Author
dc.contributor.author
Parra, Eduardo
Author
dc.contributor.author
Ferreira Parker, Jorge
Author
dc.contributor.author
Gutiérrez, Luis
Admission date
dc.date.accessioned
2019-01-29T13:56:13Z
Available date
dc.date.available
2019-01-29T13:56:13Z
Publication date
dc.date.issued
2014
Cita de ítem
dc.identifier.citation
Oncology Reports 31: 422-427, 2014
Identifier
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1021335X
Identifier
dc.identifier.issn
17912431
Identifier
dc.identifier.other
10.3892/or.2013.2829
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/160097
Abstract
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.