Exploring a Novel Mechanism of Docetaxel Resistance in Prostate Cancer

Abstract

Docetaxel (DTX), a semi-synthetic analog of paclitaxel, has emerged as the standard of care for chemotherapy of hormone-resistant prostate cancer. Docetaxel confers its anti-neoplastic activity by inhibiting microtubule depolymerization, which leads to G2/M mitotic arrest and subsequent apoptosis (1). However, most patients treated with DTX ultimately develop resistance to the drug and succumb to the disease (2). Therefore, understanding the mechanisms underlying DTX resistance is a priority area in prostate cancer research. Previously, it was reported that CXCL12/CXCR4 signaling play an important role in microtubule organization in immune cells (3) and its inhibition induced mitotic catastrophe (G2/M arrest) in ovarian cancer cells (4). Based on these earlier observations, we hypothesized that CXCL12-CXCR4 signaling axis would promote docetaxel resistance by counteracting the microtubule stabilizing action of docetaxel.

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Document Details

Document Type
Technical Report
Publication Date
Mar 01, 2013
Accession Number
ADA576367

Entities

People

  • Ajay Singh

Organizations

  • University of South Alabama

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Biomedical Research
  • Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemotherapy
  • Cytoskeleton
  • Depolymerization
  • Diseases And Disorders
  • Inhibition
  • Neoplasms
  • Ovarian Cancer
  • Polymerization
  • Prostate
  • Prostate Cancer
  • Resistance

Fields of Study

  • Chemistry

Readers

  • Molecular Biology and Genetics
  • Oncology (Cancer Research).
  • Prostate Cancer Biology.