Neuroendocrine Differentiation and Enzalutamide Resistance in Prostate Cancer

Abstract

The goal of the present proposal is to investigate the mechanism by which TCF4 regulates neuroendocrine differentiation (NED) and induces enzalutamide resistance in CRPC. In treating patients with CRPC, enzalutamide, the second-generation AR antagonist, has been considered a cornerstone of care. However, clinical benefits are limited to a median time of 4.8 months because resistance to enzalutamide inevitably emerges. Based on a body of preliminary data, we hypothesize that the transcription factor TCF4 is induced by AR-V7 and mediates, in part, enzalutamide resistance in CaP cells via the neuroendocrine marker, PTHrP. To test this hypothesis, two specific aims and four major tasks have been proposed. Of these objectives, major task 1 that focused on the role of AR and AR-V7 with TCF4 has been completed. We have found that the knockdown of AR-V7 reverses neuroendocrine differentiation and TCF4 expression. In addition, AR response element has been identified. Finally, overexpression of TCF4 has demonstrated neuroendocrine differentiation in vivo.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2018
Accession Number
AD1095880

Entities

People

  • Isaac Y. Kim

Tags

DTIC Thesaurus Topics

  • Biological Staining And Labeling
  • Biomedical Research
  • Cancer
  • Cell Count
  • Cell Line
  • Cells
  • Demographic Cohorts
  • Gene Expression
  • Molecules
  • Neoplasms
  • Prostate
  • Prostate Cancer
  • Proteins
  • Resistance
  • Tissue Culture
  • Tissues
  • Transcription Factors

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics
  • Prostate Cancer Biology.