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LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling
LMO2 is traditionally recognized as a pivotal transcriptional regulator during embryonic hematopoiesis and angionenesis, and its ectopic expression in T lymphocyte progenitors is closely correlated to the onset of acute T lymphocytic leukemia. However, recently studies revealed complicated expressio...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354749/ https://www.ncbi.nlm.nih.gov/pubmed/27880729 http://dx.doi.org/10.18632/oncotarget.13434 |
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author | Liu, Ye Wang, Zhaoyang Huang, Di Wu, Chao Li, Huihui Zhang, Xin Meng, Bin Li, Zongjin Zhu, Tianhui Yang, Shuang Sun, Wei |
author_facet | Liu, Ye Wang, Zhaoyang Huang, Di Wu, Chao Li, Huihui Zhang, Xin Meng, Bin Li, Zongjin Zhu, Tianhui Yang, Shuang Sun, Wei |
author_sort | Liu, Ye |
collection | PubMed |
description | LMO2 is traditionally recognized as a pivotal transcriptional regulator during embryonic hematopoiesis and angionenesis, and its ectopic expression in T lymphocyte progenitors is closely correlated to the onset of acute T lymphocytic leukemia. However, recently studies revealed complicated expression features and dual functions of LMO2 on tumor behaviors in a variety of cancer types, including breast cancers. Basal-type breast cancer is one of the breast cancer subtypes and a prognostically unfavorable subtype among all breast cancers. Herein we found that in basal-type breast cancer specifically, high LMO2 expression was positively correlated with lymph node metastases in patients, promoted tumor cell migration and invasion and increased distant metastasis in SCID mice. Moreover, the novel function of LMO2 was achieved by its predominantly cytoplasmic location and interaction with cofilin1, which is a critical regulator in actin cytoskeleton dynamics. These findings suggest a subtype-dependent role of LMO2 in breast cancers and the potential of LMO2 as a subtype-specific biomarker for clinical practice. |
format | Online Article Text |
id | pubmed-5354749 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-53547492017-04-14 LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling Liu, Ye Wang, Zhaoyang Huang, Di Wu, Chao Li, Huihui Zhang, Xin Meng, Bin Li, Zongjin Zhu, Tianhui Yang, Shuang Sun, Wei Oncotarget Research Paper LMO2 is traditionally recognized as a pivotal transcriptional regulator during embryonic hematopoiesis and angionenesis, and its ectopic expression in T lymphocyte progenitors is closely correlated to the onset of acute T lymphocytic leukemia. However, recently studies revealed complicated expression features and dual functions of LMO2 on tumor behaviors in a variety of cancer types, including breast cancers. Basal-type breast cancer is one of the breast cancer subtypes and a prognostically unfavorable subtype among all breast cancers. Herein we found that in basal-type breast cancer specifically, high LMO2 expression was positively correlated with lymph node metastases in patients, promoted tumor cell migration and invasion and increased distant metastasis in SCID mice. Moreover, the novel function of LMO2 was achieved by its predominantly cytoplasmic location and interaction with cofilin1, which is a critical regulator in actin cytoskeleton dynamics. These findings suggest a subtype-dependent role of LMO2 in breast cancers and the potential of LMO2 as a subtype-specific biomarker for clinical practice. Impact Journals LLC 2016-11-17 /pmc/articles/PMC5354749/ /pubmed/27880729 http://dx.doi.org/10.18632/oncotarget.13434 Text en Copyright: © 2017 Liu et al. http://creativecommons.org/licenses/by/3.0/ 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 author and source are credited. |
spellingShingle | Research Paper Liu, Ye Wang, Zhaoyang Huang, Di Wu, Chao Li, Huihui Zhang, Xin Meng, Bin Li, Zongjin Zhu, Tianhui Yang, Shuang Sun, Wei LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling |
title | LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling |
title_full | LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling |
title_fullStr | LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling |
title_full_unstemmed | LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling |
title_short | LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling |
title_sort | lmo2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354749/ https://www.ncbi.nlm.nih.gov/pubmed/27880729 http://dx.doi.org/10.18632/oncotarget.13434 |
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