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Nuclear factor I-C regulates E-cadherin via control of KLF4 in breast cancer
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Hye-Kyung | - |
dc.contributor.author | Lee, Dong-Seol | - |
dc.contributor.author | Park, Joo-Cheol | - |
dc.date.accessioned | 2017-02-08T01:09:49Z | - |
dc.date.available | 2017-02-08T01:09:49Z | - |
dc.date.issued | 2015-03-10 | - |
dc.identifier.citation | BMC Cancer, 15(1):113 | ko_KR |
dc.identifier.uri | https://hdl.handle.net/10371/100518 | - |
dc.description | This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. | ko_KR |
dc.description.abstract | Abstract
Background Progression to metastasis is the leading cause of most cancer-related mortality; however, much remains to be understood about what facilitates the spread of tumor cells. In the present study, we describe a novel pathway in breast cancer that regulates epithelial-to-mesenchymal transition (EMT), motility, and invasiveness. Methods We examined nuclear factor I-C (NFI-C) expression in MCF10A human breast epithelial cells, MCF7 non-invasive breast cancer cells, and MDA-MB231 invasive breast cancer cells by real-time PCR and western blotting. To investigate the loss- and gain-function of NFI-C, we determined whether NFI-C regulated KLF4 expression by real-time PCR, western blotting, and promoter assay. To understand the biological functions of NFI-C, we observed cell invasion, migration, adhesion in human tumor cells by transwell assay, wound healing assay, quantitative RT-PCR, cell adhesion assay, western blotting, and immunohistochemistry. Results We identified the downstream factors of NFI-C, such as KLF4 and E-cadherin, which play roles in EMT. NFI-C is expressed in normal mammary gland or noninvasive breast cancer cells with epithelial characteristics. NFI-C overexpression induced expression of KLF4 and E-cadherin, but not Slug, in breast cancer cells. NFI-C bound directly to the KLF4 promoter and stimulated KLF4 transcriptional activity, thereby regulating E-cadherin expression during tumorigenesis. Cells overexpressing NFI-C maintained their epithelial differentiation status, which could drive mesenchymal-epithelial transition (MET) via the NFI-C-KLF4-E-cadherin axis in breast cancer cells. Consequently, NFI-C suppressed EMT, migration, and invasion in breast cancer cells. Conclusions Our study reveals a novel signaling pathway that is important during breast cancer tumorigenesis: the NFI-C-KLF4-E-cadherin pathway. The results indicate the important role of NFI-C in regulating KLF4 during tumorigenesis. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BioMed Central | ko_KR |
dc.subject | NFI-C | ko_KR |
dc.subject | KLF4 | ko_KR |
dc.subject | E-cadherin | ko_KR |
dc.subject | Tumorigenesis | ko_KR |
dc.title | Nuclear factor I-C regulates E-cadherin via control of KLF4 in breast cancer | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 이혜경 | - |
dc.contributor.AlternativeAuthor | 이동설 | - |
dc.contributor.AlternativeAuthor | 박주철 | - |
dc.identifier.doi | 10.1186/s12885-015-1118-z | - |
dc.language.rfc3066 | en | - |
dc.rights.holder | Lee et al.; licensee BioMed Central. | - |
dc.date.updated | 2017-01-06T10:11:41Z | - |
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