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Nuclear factor I-C regulates E-cadherin via control of KLF4 in breast cancer

DC Field Value Language
dc.contributor.authorLee, Hye-Kyung-
dc.contributor.authorLee, Dong-Seol-
dc.contributor.authorPark, Joo-Cheol-
dc.date.accessioned2017-02-08T01:09:49Z-
dc.date.available2017-02-08T01:09:49Z-
dc.date.issued2015-03-10-
dc.identifier.citationBMC Cancer, 15(1):113ko_KR
dc.identifier.urihttps://hdl.handle.net/10371/100518-
dc.descriptionThis 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.abstractAbstract

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.isoenko_KR
dc.publisherBioMed Centralko_KR
dc.subjectNFI-Cko_KR
dc.subjectKLF4ko_KR
dc.subjectE-cadherinko_KR
dc.subjectTumorigenesisko_KR
dc.titleNuclear factor I-C regulates E-cadherin via control of KLF4 in breast cancerko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor이혜경-
dc.contributor.AlternativeAuthor이동설-
dc.contributor.AlternativeAuthor박주철-
dc.identifier.doi10.1186/s12885-015-1118-z-
dc.language.rfc3066en-
dc.rights.holderLee et al.; licensee BioMed Central.-
dc.date.updated2017-01-06T10:11:41Z-
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