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RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells
The oncogene Bmi-1 is a member of the Polycomb group gene family. Its expression is found to be greatly increased in a number of malignant tumors including breast cancer. This could suggest Bmi-1 as a potent therapeutic target. In this study, RNAi was introduced to down-regulate the expression of Bm...
Autores principales: | , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Sociedade Brasileira de Genética
2009
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3036904/ https://www.ncbi.nlm.nih.gov/pubmed/21637439 http://dx.doi.org/10.1590/S1415-47572009005000092 |
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author | Wu, Xiang-mei Liu, Xing Bu, You-quan Sengupta, Joyeeta Cui, Hong-juan Yi, Fa-ping Liu, Tao Yuan, Chen-fu Shi, Yan-yan Song, Fang-zhou |
author_facet | Wu, Xiang-mei Liu, Xing Bu, You-quan Sengupta, Joyeeta Cui, Hong-juan Yi, Fa-ping Liu, Tao Yuan, Chen-fu Shi, Yan-yan Song, Fang-zhou |
author_sort | Wu, Xiang-mei |
collection | PubMed |
description | The oncogene Bmi-1 is a member of the Polycomb group gene family. Its expression is found to be greatly increased in a number of malignant tumors including breast cancer. This could suggest Bmi-1 as a potent therapeutic target. In this study, RNAi was introduced to down-regulate the expression of Bmi-1 in a highly malignant breast adenocarcinoma cell line, MCF-7. A thorough study of the biological behavior and chemosensitivity changes of the MCF-7 cells was carried out in context to the therapeutic potential of Bmi-1. The results obtained indicated that siRNA targeting of Bmi-1 could lead to an efficient and specific inhibition of endogenous Bmi-1 activity. The mRNA and protein expression of Bmi-1 were determined by RT-PCR and Western blot, respectively. Furthermore, silencing of Bmi-1 resulted in a drastic inhibition of the growth of MCF-7 cells as well as G(1) /S phase transition. The number of target cells was found to increase in phase G (0) /G (1) and decrease in the S phase, but no increase in the basal level of apoptosis was noticed. On the other hand, a reduction in the expression of cyclin D1 and an increase in the expression of p21 were also noticed. Silencing of Bmi-1 made the MCF-7 cells more sensitive to the chemotherapeutic agent doxorubicin and induced a significantly higher percentage of apoptotic cells. Here, we report on a study regarding the RNAi-mediated silencing of the Bmi-1 gene in breast cancer. |
format | Text |
id | pubmed-3036904 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Sociedade Brasileira de Genética |
record_format | MEDLINE/PubMed |
spelling | pubmed-30369042011-06-02 RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells Wu, Xiang-mei Liu, Xing Bu, You-quan Sengupta, Joyeeta Cui, Hong-juan Yi, Fa-ping Liu, Tao Yuan, Chen-fu Shi, Yan-yan Song, Fang-zhou Genet Mol Biol Human and Medical Genetics The oncogene Bmi-1 is a member of the Polycomb group gene family. Its expression is found to be greatly increased in a number of malignant tumors including breast cancer. This could suggest Bmi-1 as a potent therapeutic target. In this study, RNAi was introduced to down-regulate the expression of Bmi-1 in a highly malignant breast adenocarcinoma cell line, MCF-7. A thorough study of the biological behavior and chemosensitivity changes of the MCF-7 cells was carried out in context to the therapeutic potential of Bmi-1. The results obtained indicated that siRNA targeting of Bmi-1 could lead to an efficient and specific inhibition of endogenous Bmi-1 activity. The mRNA and protein expression of Bmi-1 were determined by RT-PCR and Western blot, respectively. Furthermore, silencing of Bmi-1 resulted in a drastic inhibition of the growth of MCF-7 cells as well as G(1) /S phase transition. The number of target cells was found to increase in phase G (0) /G (1) and decrease in the S phase, but no increase in the basal level of apoptosis was noticed. On the other hand, a reduction in the expression of cyclin D1 and an increase in the expression of p21 were also noticed. Silencing of Bmi-1 made the MCF-7 cells more sensitive to the chemotherapeutic agent doxorubicin and induced a significantly higher percentage of apoptotic cells. Here, we report on a study regarding the RNAi-mediated silencing of the Bmi-1 gene in breast cancer. Sociedade Brasileira de Genética 2009 2009-12-01 /pmc/articles/PMC3036904/ /pubmed/21637439 http://dx.doi.org/10.1590/S1415-47572009005000092 Text en Copyright © 2009, Sociedade Brasileira de Genética. http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Human and Medical Genetics Wu, Xiang-mei Liu, Xing Bu, You-quan Sengupta, Joyeeta Cui, Hong-juan Yi, Fa-ping Liu, Tao Yuan, Chen-fu Shi, Yan-yan Song, Fang-zhou RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells |
title | RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells |
title_full | RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells |
title_fullStr | RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells |
title_full_unstemmed | RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells |
title_short | RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells |
title_sort | rnai-mediated silencing of the bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in mcf-7 cells |
topic | Human and Medical Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3036904/ https://www.ncbi.nlm.nih.gov/pubmed/21637439 http://dx.doi.org/10.1590/S1415-47572009005000092 |
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