Time depended Bcl-2 inhibition might be useful for a targeted drug therapy. Issue 1 (December 2015)

• Record Type: Journal Article
• Authors: Talaiezadeh, Abdolhassan; jalali, Fateme; Galehdari, Hamid; Khodadadi, Ali
• Is Part Of: Cancer cell international. Volume 15:Issue 1(2015)
• Page Start: 1
• Page End: 7
• Publication Date: 2015-12
• Subjects: Small interfering RNA -- Apoptosis -- Autophagy -- Gene silencing -- Nanoparticles; Cytology -- Periodicals; 616.994
• DOI: 10.1186/s12935-015-0254-5
• Languages: English
• ISSNs: 1475-2867

Abstract

Background Over expression of Bcl-2 is frequently observed in several types of cancers and it is one of the prognostic markers in breast cancer. The importance of the Bcl-2 protein as ideal therapeutic target is the dual role of inhibiting apoptosis and autophagy-mediated cell death. Thus, the bcl-2 targeting may be a strategy of choice to improve treatment efficacy and overcome drug resistance to cancer chemotherapy. For this reason, we designed the siRNA mediated silencing of the Bcl-2 gene in the MCF-7 breast cancer cell line. Objectives The purpose of this research was to investigate the effective Bcl-2 gene silencing by our homemade siRNA, more than previous study. Our data demonstrated that specific inhibition of the Bcl-2 by siRNA induces approximately more than 90 % gene silencing. Methods MCF-7 Cell lines were treated by homemade Bcl-2siRNA for the first time and control siRNA that was transfected with nanoparticle. The cells harvested at 24, 48 and 72 h and transcription level of Bcl-2 was examined by Real Time -PCR analysis. The drug sensitivity was detected by using LDH assay test. Finally Anexin V-FITC test was performed for evaluation of apoptosis. Results In the present study, results showed that targeting the specific sequence of the Bcl-2 by our homemade siRNA in the MCF7 cell line and its effect was more obvious in 24 h in contrast to 48 and 72 h. Conclusions However, we showed here a time dependent blocking of the bcl-2 transcript that might lead to cell dead due autophagy, and not necessarily to apoptosis.