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Article

Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor

  • Authors:
    • Eduardo Parra
    • Luis Gutiérrez
    • Jorge Ferreira
  • View Affiliations / Copyright

    Affiliations: Laboratory of Experimental Biomedicine, University of Tarapaca, Campus Esmeralda, Iquique, Chile, Faculty of Sciences, Arturo Prat University, Iquique, Chile, Programme of Molecular and Clinical Pharmacology, ICBM, Medical Faculty, University of Chile, Santiago, Chile
  • Pages: 911-916
    |
    Published online on: May 28, 2013
       https://doi.org/10.3892/or.2013.2503
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Abstract

The p21Waf1/Cip1 protein (hereafter, p21) and the c‑Jun N-terminal kinase (JNK) are two well-characterized cell modulators that play a crucial role in cell differentiation, senescence and apoptosis. Here, we report that transcription of the p21Waf1/Cip1 and JNK-1 genes is affected by inhibition of the early growth response-1 (Egr-1) in response to a small interfering RNA [siRNA)-Egr-1] in LNCaP and PC-3 prostate carcinoma cell lines. The expression levels of protein were determined by western blotting, and apoptosis was measured by propidium iodide staining and flow cytometric analysis. Inhibition of Egr-1, p21 and JNK-1 was carried out by siRNAs. LNCaP and PC-3 cells exhibited readily detectable Egr-1, JNK and p21, even in low serum medium without the addition of other exogenous agents. The expression of Egr-1, p21 and JNK was strongly increased after treatment of the cells with TPA, tumor necrosis factor-α (TNF-α) or arsenite. Suppression of Egr-1 expression by siRNA abrogated the ability of TPA to induce Egr-1 and JNK-1 activities, moderately increasing the p21 activity and abrogating the anti-apoptotic effect of Egr-1 observed in the prostate cancer cell lines. Moreover, blockade of p21 and JNK was unable to decrease the activity of Egr-1, while siRNA against p21 abrogated the pro‑apoptotic effect of p21. The results demonstrated that Egr-1 acts as a key player in prostate tumor cell growth and survival, while p21 plays a key pro‑apoptotic role in LNCaP and PC-3 prostate carcinoma cell lines.
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Copy and paste a formatted citation
Spandidos Publications style
Parra E, Gutiérrez L and Ferreira J: Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor. Oncol Rep 30: 911-916, 2013.
APA
Parra, E., Gutiérrez, L., & Ferreira, J. (2013). Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor. Oncology Reports, 30, 911-916. https://doi.org/10.3892/or.2013.2503
MLA
Parra, E., Gutiérrez, L., Ferreira, J."Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor". Oncology Reports 30.2 (2013): 911-916.
Chicago
Parra, E., Gutiérrez, L., Ferreira, J."Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor". Oncology Reports 30, no. 2 (2013): 911-916. https://doi.org/10.3892/or.2013.2503
Copy and paste a formatted citation
x
Spandidos Publications style
Parra E, Gutiérrez L and Ferreira J: Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor. Oncol Rep 30: 911-916, 2013.
APA
Parra, E., Gutiérrez, L., & Ferreira, J. (2013). Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor. Oncology Reports, 30, 911-916. https://doi.org/10.3892/or.2013.2503
MLA
Parra, E., Gutiérrez, L., Ferreira, J."Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor". Oncology Reports 30.2 (2013): 911-916.
Chicago
Parra, E., Gutiérrez, L., Ferreira, J."Increased expression of p21Waf1/Cip1 and JNK with costimulation of prostate cancer cell activation by an siRNA Egr-1 inhibitor". Oncology Reports 30, no. 2 (2013): 911-916. https://doi.org/10.3892/or.2013.2503
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