Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5509422 | Cellular Signalling | 2016 | 26 Pages |
Abstract
WD repeat domain 1 (WDR1), a protein that assists cofilin-mediated actin filament disassembly, is overexpressed in the invading front of invasive ductal carcinoma (IDC), but its implication of overexpression and how to be regulated have not been studied. In our study, we demonstrated that STAT3 bound to the 5â² upstream sequence (â 1971 to â 1964), a putative promoter region, of WDR1 gene, and its activation induced WDR1 overexpression in breast cancer cells. The exogenous overexpression of WDR1 increased the migration of MDA-MB-231, which was attenuated by WDR1 knockdown. In the analysis of breast cancer patients, WDR1 overexpression was associated with a shorter distant metastasis-free survival (DMFS), more specifically in basal-like tumors.
Keywords
DMFSSTAT3BCCIL-6F-actinDCISFBSIDCfilamentous actinFFPEchromatin immunoprecipitationIHCImmunohistochemistryinterleukin-6Breast cancerfetal bovine serumBreast cancer cellTranscription factorformalin-fixed, paraffin-embeddedsignal transducer and activator of transcription 3Cell migrationCHiPDuctal carcinoma in situInvasive ductal carcinoma
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Authors
Joo Hyun Lee, Ji Eun Kim, Baek Gil Kim, Hyun Ho Han, Suki Kang, Nam Hoon Cho,