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Effects and mechanism of downregulation of COX-2 expression by RNA interference on proliferation and apoptosis of human breast cancer MCF-7 cells.
- Source :
-
Molecular Medicine Reports . 2014, Vol. 10 Issue 6, p3092-3098. 7p. - Publication Year :
- 2014
-
Abstract
- The aim of the present study was to investigate the effects of RNA interference with prostaglandin-endoperoxide synthase 2 (COX-2) gene on the proliferation and apoptosis of breast cancer MCF-7 cells, as well as the underlying mechanism. The present study constructed the eukaryotic expression vector of the targeted COX-2 gene, transfected the MCF-7 cells and screened the stably expressed clone. Changes in the COX-2 gene expression in breast cancer MCF-7 cells prior to and following transfection were examined; the proliferation and apoptosis of MCF-7 cells were analyzed. Furthermore, changes in the protein levels of survivin, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (Bax) genes were detected. RNA interference mediated by a lentiviral expression vector significantly decreased the protein expression levels of the COX-2 gene, and therefore, the proliferation and growth of breast cancer MCF-7 cells was significantly suppressed and the apoptotic rate increased. Of note, the mRNA and protein expression levels of survivin and Bcl-2 decreased, while those of Bax increased following COX-2 silencing. RNA interference markedly deactivated the COX-2 gene, suppressed the proliferation of breast cancer MCF-7 cells, and, to a certain extent, enhanced the induced spontaneous apoptosis, which is regulated by the Bax gene. These results provided evidence for the potential applications of RNA interference of the targeted COX-2 gene in gene therapy for the treatment of breast cancer. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 17912997
- Volume :
- 10
- Issue :
- 6
- Database :
- Academic Search Index
- Journal :
- Molecular Medicine Reports
- Publication Type :
- Academic Journal
- Accession number :
- 99898665
- Full Text :
- https://doi.org/10.3892/mmr.2014.2659