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UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer
BACKGROUND: Ubiquitin-associated protein 2-like (UBAP2L) contains a ubiquitin-associated domain near its N-terminus, which has been demonstrated to be overexpressed in multiple tumors, including hepatocellular carcinoma and colorectal carcinoma but its role has not been well studied in breast cancer...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Japan
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5818569/ https://www.ncbi.nlm.nih.gov/pubmed/29196913 http://dx.doi.org/10.1007/s12282-017-0820-x |
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author | He, Jing Chen, Yuanping Cai, Lu Li, Zelei Guo, Xiaoqing |
author_facet | He, Jing Chen, Yuanping Cai, Lu Li, Zelei Guo, Xiaoqing |
author_sort | He, Jing |
collection | PubMed |
description | BACKGROUND: Ubiquitin-associated protein 2-like (UBAP2L) contains a ubiquitin-associated domain near its N-terminus, which has been demonstrated to be overexpressed in multiple tumors, including hepatocellular carcinoma and colorectal carcinoma but its role has not been well studied in breast cancer. Thus, this study was designed to evaluate whether UBAP2L can serve as a potential molecular target for breast cancer therapy. METHODS: The expression of UBAP2L was determined in breast cancer tissues and cell lines by Western blotting and Oncomine database mining. Then the expression of UBAP2L was silenced using RNA interference and the effects of UBAP2L knockdown on breast cancer cell proliferation and cell cycle progression by MTT and colony formation assay, and Flow cytometry, respectively. RESULTS: We found the expression of UBAP2L was significantly up-regulated in breast cancer tissues and cell lines. Knockdown of UBAP2L suppressed cell proliferation, impaired colony formation ability and induced cell cycle arrest at G2/M phase. At molecular levels, knockdown of UBAP2L increased p21 expression, but decreased the expression of CDK1 and Cyclin B1 in breast cancer cells. CONCLUSION: Our findings suggest that UBAP2L plays an important role in breast cancer cell proliferation and might serve as a potential target for breast cancer treatment. |
format | Online Article Text |
id | pubmed-5818569 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Springer Japan |
record_format | MEDLINE/PubMed |
spelling | pubmed-58185692018-02-27 UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer He, Jing Chen, Yuanping Cai, Lu Li, Zelei Guo, Xiaoqing Breast Cancer Original Article BACKGROUND: Ubiquitin-associated protein 2-like (UBAP2L) contains a ubiquitin-associated domain near its N-terminus, which has been demonstrated to be overexpressed in multiple tumors, including hepatocellular carcinoma and colorectal carcinoma but its role has not been well studied in breast cancer. Thus, this study was designed to evaluate whether UBAP2L can serve as a potential molecular target for breast cancer therapy. METHODS: The expression of UBAP2L was determined in breast cancer tissues and cell lines by Western blotting and Oncomine database mining. Then the expression of UBAP2L was silenced using RNA interference and the effects of UBAP2L knockdown on breast cancer cell proliferation and cell cycle progression by MTT and colony formation assay, and Flow cytometry, respectively. RESULTS: We found the expression of UBAP2L was significantly up-regulated in breast cancer tissues and cell lines. Knockdown of UBAP2L suppressed cell proliferation, impaired colony formation ability and induced cell cycle arrest at G2/M phase. At molecular levels, knockdown of UBAP2L increased p21 expression, but decreased the expression of CDK1 and Cyclin B1 in breast cancer cells. CONCLUSION: Our findings suggest that UBAP2L plays an important role in breast cancer cell proliferation and might serve as a potential target for breast cancer treatment. Springer Japan 2017-12-01 2018 /pmc/articles/PMC5818569/ /pubmed/29196913 http://dx.doi.org/10.1007/s12282-017-0820-x Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Original Article He, Jing Chen, Yuanping Cai, Lu Li, Zelei Guo, Xiaoqing UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer |
title | UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer |
title_full | UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer |
title_fullStr | UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer |
title_full_unstemmed | UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer |
title_short | UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer |
title_sort | ubap2l silencing inhibits cell proliferation and g2/m phase transition in breast cancer |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5818569/ https://www.ncbi.nlm.nih.gov/pubmed/29196913 http://dx.doi.org/10.1007/s12282-017-0820-x |
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