Effects of Phthalates on Androgen Receptor Regulation Associated with Castration-Resistant Prostate Cancer Development

Abstract

Prostate cancer is one of the leading causes of death for men in the United States. Initially, prostate cancer patients are treated with androgen deprivation therapy. This treatment is usually successful at first; however, prostate cancer can recur years later as castration resistant prostate cancer (CRPC). CRPC is much more aggressive and is frequently lethal. Despite the immense clinical significance of CRPC, little is known about the molecular mechanisms that cause prostate cancer to become castration-resistant. We have found that the RNA helicase DDX3 plays a critical role in translational control of the androgen receptor (AR) in CRPC, highlighting a new mechanism by which prostate cancer becomes castration resistant. Future efforts will be dedicated to determining if DDX3-dependent translational control plays a role in phthalate-triggered reduction of AR in prostate cancer.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2018
Accession Number
AD1093751

Entities

People

  • Sarah Neuman

Organizations

  • University of Wisconsin System

Tags

DTIC Thesaurus Topics

  • Androgen Receptors
  • Androgens
  • Castration
  • Cell Line
  • Cells
  • Deprivation
  • Drosophila
  • Molecules
  • Neoplasms
  • Phthalates
  • Prostate
  • Prostate Cancer
  • Proteins
  • Small Molecules
  • Therapy
  • Tissues
  • United States

Readers

  • Molecular and genetic basis of cancer.
  • Oncology (Cancer Research).