Inhibition of Early Growth Response 1 by a Specific siRNA Modulates the Expression of p21Waf1/Cip1 and JNK-1 Proteins in Prostate PC-3 and LNCaP Carcinoma Cell Lines | Chapter 11 | Advanced Research in Biological Science Vol. 4

 This study accompanied that blocking of Egr-1 expres- sion by a limited interfering RNA (siRNA-Egr-1) raised the activity of p21Waf1/Cip1 and declined the expression of JNK protein. In contrast, siRNA muffling of p21 or JNK-1 with siRNAs was impotent to decrease the expression of Egr-1. The p21Waf1/Cip1 protein (hereafter, p21) and the c-Jun N-terminal kinase (JNK) are two well-typified cell modulators that play a critical role in container differentiation, agedness, and apoptosis. Here, we report that transcription of the p21Waf1/Cip1 and JNK-1 genes is distressed by inhibition of the early tumor response-1 (Egr-1) in reaction to a small meddling RNA [siRNA)-Egr-1] in LNCaP and PC-3 prostate carcinoma container lines. The expression levels of protein were contingent upon western blotting, and apoptosis was calculated by propidium iodide staining and flow cytometric analysis. Inhibition of Egr-1, p21 and JNK-1 was completed activity by siRNAs. LNCaP and PC-3 cells shown readily perceptible Egr-1, JNK and p21, even in low antitoxin medium without the adding of other exogenic agents. The verbalization of Egr-1, p21 and JNK was strongly raised after situation of the cells accompanying TPA, tumor fatality factor-α (TNF-α) or arsenite. Suppression of Egr-1 verbalization by siRNA abrogated the ability of TPA to encourage Egr-1 and JNK-1 activities, rather increasing the p21 endeavor and abrogating the antagonistic-apoptotic effect of Egr-1 observed in the prostate malignancy cell lines. Moreover, barrier of p21 and JNK was unable to decrease the exercise of Egr-1, while siRNA against p21 abrogated the pro-apoptotic effect of p21. The results explained that Egr-1 acts as a key player in prostate Cancer cell progress and survival, while p21 plays a key supporting-apoptotic role in LNCaP and PC-3 prostate malignant growth cell lines.

Author(s) Details:

Eduardo Parra,
Biomedical Experimental Laboratory, Faculty of Medicine, Campus Saucache, University of Tarapacá, Avenida Senador Luis Valente Rossi 2223, Arica, Chile.

Victor Rojas,
Facultad de Ciencias Agrarias y Forestales, Programa de Doctorado en Biotecnología Traslacional, Universidad Católica del Maule, Ave. San Miguel 3605, Talca, Chile.

Jorge Ferreira,
Programme of Molecular and Clinical Pharmacology, ICBM, Medical Faculty, University of Chile, Avenida Indenpendencia 1027, Independencia, Santiago, Chile.

Please see the link here: https://stm.bookpi.org/ARBS-V4/article/view/11980