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Accepted (AM)Open Access (License Unspecified), Open
Journal article
Cell Fate Factor DACH1 Represses YB-1-mediated Oncogenic Transcription and Translation
Cancer research (Chicago, Ill.), v 74(3), pp 829-839
12 Dec 2013
PMID: 24335958
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The epithelial-mesenchymal transition (EMT) enhances cellular invasiveness and confers tumor cells with cancer stem cell like characteristics, through transcriptional and translational mechanisms. The mechanisms maintaining transcriptional and translational repression of EMT and cellular invasion are poorly understood. Herein, the cell fate-determination factor Dachshund (DACH1), suppressed EMT via repression of cytoplasmic translational induction of Snail by inactivating the Y box-binding protein (YB-1). In the nucleus, DACH1 antagonized YB-1-mediated oncogenic transcriptional modules governing cell invasion. DACH1 blocked YB-1-induced mammary tumor growth and EMT in mice. In basal-like breast cancer (BLBC) the reduced expression of DACH1 and increased YB-1, correlated with poor metastasis free survival. The loss of DACH1 suppression of both cytoplasmic translational and nuclear transcriptional events governing EMT and tumor invasion may contribute to poor prognosis in basal-like forms of breast cancer, a relatively aggressive disease subtype.
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Details
- Title
- Cell Fate Factor DACH1 Represses YB-1-mediated Oncogenic Transcription and Translation
- Creators
- Kongming Wu - Thomas Jefferson UniversityKe Chen - Thomas Jefferson UniversityChenguang Wang - Thomas Jefferson UniversityXuanmao Jiao - Thomas Jefferson UniversityLiping Wang - Thomas Jefferson UniversityJie Zhou - Kimmel Cancer CenterJing Wang - Tongji Medical CollegeZhiping Li - Kimmel Cancer CenterSankar Addya - Thomas Jefferson UniversityPoul H. Sorensen - BC Cancer Research CentreMichael P. Lisanti - Breast Cancer Research FoundationAndrew Quong - LeidosAdam Ertel - Thomas Jefferson UniversityRichard G. Pestell - Thomas Jefferson University
- Publication Details
- Cancer research (Chicago, Ill.), v 74(3), pp 829-839
- Publisher
- American Association for Cancer Research (AACR)
- Grant note
- R01 CA086072 || CA / National Cancer Institute : NCI P30 CA056036 || CA / National Cancer Institute : NCI R01 CA070896 || CA / National Cancer Institute : NCI R01 CA075503 || CA / National Cancer Institute : NCI R01 CA132115 || CA / National Cancer Institute : NCI
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- School of Biomedical Engineering, Science, and Health Systems
- Web of Science ID
- WOS:000331073900020
- Scopus ID
- 2-s2.0-84893834114
- Other Identifier
- 991019176798404721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Oncology