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Article

Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product

  • Authors:
    • Eduardo Parra
    • Luís Gutierréz
    • Jorge Ferreira
  • View Affiliations / Copyright

    Affiliations: Laboratory of Experimental Biomedicine, University of Tarapaca, Campus Esmeralda, Iquique, Chile, Faculty of Sciences, University Arturo Prat, Iquique, Chile, Programme of Molecular and Clinical Pharmacology, ICBM, Medical Faculty, University of Chile, Santiago, Chile
  • Pages: 1163-1169
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    Published online on: November 16, 2015
       https://doi.org/10.3892/or.2015.4424
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Abstract

The Tax protein of human T cell leukemia virus type 1 plays a major role in the pathogenesis of adult T cell leukemia (ATL), an aggressive neoplasia of CD4+ T cells. In the present study, we investigated whether the EGR-1 pathway is involved in the regulation of Tax-induced JNK expression in human Jurkat T cells transfected to express the Tax protein in the presence or absence of PMA or ionomycin. Overexpression of EGR-1 in Jurkat cells transfected to express Tax, promoted the activation of several genes, with the most potent being those that contained AP-1 (Jun/c-Fos), whereas knockdown of endogenous EGR-1 by small interfering RNA (siRNA) somewhat reduced Tax-mediated JNK-1 transcription. Additionally, luciferase-based AP-1 and NF-κB reporter gene assays demonstrated that inhibition of EGR-1 expression by an siRNA did not affect the transcriptional activity of a consensus sequence of either AP-1 or NF-κB. On the other hand, the apoptosis assay, using all-trans retinoic acid (ATRA) as an inducer of apoptosis, confirmed that siRNA against EGR-1 failed to suppress ATRA-induced apoptosis in Jurkat and Jurkat-Tax cells, as noted by the low levels of both DEVDase activity and DNA fragmentation, indicating that the induction of apoptosis by ATRA was Egr-1-independent. Finally, our data showed that activation of Tax by JNK-1 was not dependent on the EGR-1 cascade of events, suggesting that EGR-1 is important but not a determinant for the activity for Tax-induced proliferation of Jurkat cells.
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Copy and paste a formatted citation
Spandidos Publications style
Parra E, Gutierréz L and Ferreira J: Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product. Oncol Rep 35: 1163-1169, 2016.
APA
Parra, E., Gutierréz, L., & Ferreira, J. (2016). Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product. Oncology Reports, 35, 1163-1169. https://doi.org/10.3892/or.2015.4424
MLA
Parra, E., Gutierréz, L., Ferreira, J."Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product". Oncology Reports 35.2 (2016): 1163-1169.
Chicago
Parra, E., Gutierréz, L., Ferreira, J."Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product". Oncology Reports 35, no. 2 (2016): 1163-1169. https://doi.org/10.3892/or.2015.4424
Copy and paste a formatted citation
x
Spandidos Publications style
Parra E, Gutierréz L and Ferreira J: Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product. Oncol Rep 35: 1163-1169, 2016.
APA
Parra, E., Gutierréz, L., & Ferreira, J. (2016). Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product. Oncology Reports, 35, 1163-1169. https://doi.org/10.3892/or.2015.4424
MLA
Parra, E., Gutierréz, L., Ferreira, J."Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product". Oncology Reports 35.2 (2016): 1163-1169.
Chicago
Parra, E., Gutierréz, L., Ferreira, J."Activation of Tax protein by c-Jun-N-terminal kinase is not dependent on the presence or absence of the early growth response-1 gene product". Oncology Reports 35, no. 2 (2016): 1163-1169. https://doi.org/10.3892/or.2015.4424
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