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Author Notes:

Corresponding authors: Dr. Daqing Wu (dwu2@emory.edu), Department of Urology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, USA; Dr. Haiyen E. Zhau (Haiyen.Zhau@cshs.org), Uro-Oncology Research Program, Cedars-Sinai Medical Center, Los Angeles, CA, USA



  • epithelial-mesenchymal transition
  • prostate cancer
  • lymph node metastasis
  • cytoskeleton

EPLIN Downregulation Promotes Epithelial-Mesenchymal Transition in Prostate Cancer Cells and Correlates With Clinical Lymph Node Metastasis

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Journal Title:



Volume 30, Number 50


, Pages 4941-4952

Type of Work:

Article | Final Publisher PDF


Epithelial-mesenchymal transition (EMT) is a crucial mechanism for the acquisition of migratory and invasive capabilities by epithelial cancer cells. By conducting quantitative proteomics in experimental models of human prostate cancer (PCa) metastasis, we observed strikingly decreased expression of EPLIN (epithelial protein lost in neoplasm; or LIM domain and actin binding 1, LIMA-1) upon EMT. Biochemical and functional analyses demonstrated that EPLIN is a negative regulator of EMT and invasiveness in PCa cells. EPLIN depletion resulted in the disassembly of adherens junctions, structurally distinct actin remodeling, and activation of β-catenin signaling. Microarray expression analysis identified a subset of putative EPLIN target genes associated with EMT, invasion and metastasis. By immunohistochemistry EPLIN downregulation was also demonstrated in lymph node metastases of human solid tumors including PCa, breast cancer, colorectal cancer and squamous cell carcinoma of the head and neck. This study reveals a novel molecular mechanism for converting cancer cells into a highly invasive and malignant form, and has important implications in prognosing and treating metastasis at early stages.
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