Overcoming Drug Resistant Prostate Cancer with APE1/Ref-1 Blockade

Abstract

We have identified a new target that might explain how advanced prostate cancer cells avoid being killed by chemotherapy: Apurinic/apyrimidinic endonuclease/redox-factor 1, or simply, Ref-1, for short. In this report, we provide evidence that APE1/Ref-1 is induced in prostate cancer cells and in human prostate cancer. This expression correlates to inflammation and to survivin signaling in human prostate cancer specimens. Genetic knockdown of APE1/Ref-1 disrupts prostate cancer cell growth and survival in cell culture. In addition, inhibition of the redox function selectively of Ref-1 results in cell growth inhibition, with this therapy preferentially inhibiting prostate cancer cell growth above that in non-cancerous cells. Specific blockade of Ref-1 redox activity in tumors is a novel concept in tumor therapy. If we are successful, we will have defined a critical therapeutic target for drug-resistant prostate cancers, and logically clinical trials would follow targeting this pathway.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2015
Accession Number
AD1005310

Entities

People

  • Travis J. Jerde

Tags

DTIC Thesaurus Topics

  • Biomedical Research
  • Cell Line
  • Cells
  • Chemotherapy
  • Clinical Trials
  • Computer Programs
  • Culture Techniques
  • Diseases And Disorders
  • Drug Resistance
  • Inflammation
  • Inhibition
  • Inhibitors
  • Neoplasms
  • Prostate Cancer
  • Survival
  • Therapy
  • Tissues

Fields of Study

  • Biology
  • Chemistry
  • Medicine

Readers

  • Oncology and Biomarker-Based Cancer Detection.
  • Prostate Cancer Biology.

Technology Areas

  • Biotechnology
  • Biotechnology - Cancer Biotech