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Cell fate factor DACH1 represses YB-1-mediated oncogenic transcription and translation

Kongming Wu1, Ke Chen, Chenguang Wang

  • 1Authors' Affiliations: Department of Cancer Biology; Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania; Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China; and Department of Molecular Oncology, British Columbia Cancer Research Center, Vancouver, British Columbia, Canada.

Cancer Research
|December 17, 2013
PubMed

Insights

Dachshund (DACH1) protein suppresses cancer cell invasion and metastasis by inhibiting the Y box-binding protein (YB-1). Reduced DACH1 expression correlates with poor survival in aggressive breast cancers.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Epithelial-mesenchymal transition (EMT) increases cancer cell invasiveness and stem-like properties via transcriptional and translational regulation.
  • Mechanisms suppressing EMT and invasion are not well understood.

Purpose of the Study:

  • To investigate the role of Dachshund (DACH1) in regulating EMT and cancer cell invasion.
  • To elucidate the molecular mechanisms by which DACH1 suppresses EMT and invasion.

Main Methods:

  • Investigated DACH1's interaction with Y box-binding protein (YB-1) in regulating Snail translation.
  • Analyzed DACH1's effect on YB-1-mediated transcriptional activity in vitro.
  • Assessed the impact of DACH1 on mammary tumor growth and EMT in mouse models.
  • Correlated DACH1 and YB-1 expression with patient survival in basal-like breast cancer.

Main Results:

  • DACH1 inhibited cytoplasmic translational induction of Snail by inactivating YB-1.
  • DACH1 antagonized YB-1-mediated nuclear transcriptional modules driving cell invasion.
  • DACH1 suppressed YB-1-induced mammary tumor growth and EMT in mice.
  • Reduced DACH1 and increased YB-1 expression correlated with poor metastasis-free survival in basal-like breast cancer.

Conclusions:

  • DACH1 suppresses EMT and tumor invasion through both cytoplasmic translational and nuclear transcriptional repression of YB-1.
  • Loss of DACH1's suppressive function contributes to poor prognosis in aggressive basal-like breast cancers.

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