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BMI‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes
Breast cancer is among the most common malignant cancers in women. B‐cell‐specific Moloney murine leukemia virus integration site 1 (BMI‐1) is a transcriptional repressor that has been shown to be involved in tumorigenesis, the cell cycle, and stem cell maintenance. In our study, increased expressio...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9899611/ https://www.ncbi.nlm.nih.gov/pubmed/36285479 http://dx.doi.org/10.1111/cas.15623 |
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author | Liu, Jin‐yan Jiang, Yan‐nan Huang, Hai Xu, Jin‐fu Wu, Ying‐hui Wang, Qiang Zhu, Yue Zheng, Bo Shen, Cong Qian, Wei‐feng Shen, Jun |
author_facet | Liu, Jin‐yan Jiang, Yan‐nan Huang, Hai Xu, Jin‐fu Wu, Ying‐hui Wang, Qiang Zhu, Yue Zheng, Bo Shen, Cong Qian, Wei‐feng Shen, Jun |
author_sort | Liu, Jin‐yan |
collection | PubMed |
description | Breast cancer is among the most common malignant cancers in women. B‐cell‐specific Moloney murine leukemia virus integration site 1 (BMI‐1) is a transcriptional repressor that has been shown to be involved in tumorigenesis, the cell cycle, and stem cell maintenance. In our study, increased expression of BMI‐1 was found in both human triple negative breast cancer and luminal A‐type breast cancer tissues compared with adjacent tissues. We also found that knockdown of BMI‐1 significantly suppressed cell proliferation and migration in vitro and in vivo. Further mechanistic research demonstrated that BMI‐1 directly bound to the promoter region of CDKN2D/BRCA1 and inhibited its transcription in MCF‐7/MDA‐MB‐231. More importantly, we discovered that knockdown of CDKN2D/BRCA1 could promote cell proliferation and migration after repression by PTC‐209. Our results reveal that BMI‐1 transcriptionally suppressed BRCA1 in TNBC cell lines whereas, in luminal A cell lines, CDKN2D was the target gene. This provides a reference for the precise treatment of different types of breast cancer in clinical practice. |
format | Online Article Text |
id | pubmed-9899611 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-98996112023-02-09 BMI‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes Liu, Jin‐yan Jiang, Yan‐nan Huang, Hai Xu, Jin‐fu Wu, Ying‐hui Wang, Qiang Zhu, Yue Zheng, Bo Shen, Cong Qian, Wei‐feng Shen, Jun Cancer Sci Original Articles Breast cancer is among the most common malignant cancers in women. B‐cell‐specific Moloney murine leukemia virus integration site 1 (BMI‐1) is a transcriptional repressor that has been shown to be involved in tumorigenesis, the cell cycle, and stem cell maintenance. In our study, increased expression of BMI‐1 was found in both human triple negative breast cancer and luminal A‐type breast cancer tissues compared with adjacent tissues. We also found that knockdown of BMI‐1 significantly suppressed cell proliferation and migration in vitro and in vivo. Further mechanistic research demonstrated that BMI‐1 directly bound to the promoter region of CDKN2D/BRCA1 and inhibited its transcription in MCF‐7/MDA‐MB‐231. More importantly, we discovered that knockdown of CDKN2D/BRCA1 could promote cell proliferation and migration after repression by PTC‐209. Our results reveal that BMI‐1 transcriptionally suppressed BRCA1 in TNBC cell lines whereas, in luminal A cell lines, CDKN2D was the target gene. This provides a reference for the precise treatment of different types of breast cancer in clinical practice. John Wiley and Sons Inc. 2022-11-10 /pmc/articles/PMC9899611/ /pubmed/36285479 http://dx.doi.org/10.1111/cas.15623 Text en © 2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Original Articles Liu, Jin‐yan Jiang, Yan‐nan Huang, Hai Xu, Jin‐fu Wu, Ying‐hui Wang, Qiang Zhu, Yue Zheng, Bo Shen, Cong Qian, Wei‐feng Shen, Jun BMI‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes |
title |
BMI‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes |
title_full |
BMI‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes |
title_fullStr |
BMI‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes |
title_full_unstemmed |
BMI‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes |
title_short |
BMI‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes |
title_sort | bmi‐1 promotes breast cancer proliferation and metastasis through different mechanisms in different subtypes |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9899611/ https://www.ncbi.nlm.nih.gov/pubmed/36285479 http://dx.doi.org/10.1111/cas.15623 |
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