Interleukin-24 Transduction Modulates Human Prostate Cancer Malignancy Mediated by Regulation of Anchorage Dependence

Anticancer Res. 2019 Jul;39(7):3719-3725. doi: 10.21873/anticanres.13520.

Abstract

Background: Hormone therapy and chemotherapy are not effective for castrate-resistant prostate cancer, thus development of novel treatment strategies is required. Gene therapy involving transient high-copy transfection of interleukin (IL)-24 with an adenoviral vector can exert antitumor activity; however, the effects of stable IL-24 transfection are not fully understood. The aim of this study was to investigate the effects of IL-24 overexpression in prostate cancer cells, in vitro.

Materials and methods: DU145 cells were transfected the IL-24 gene using a retroviral vector. Apoptosis induction was investigated by the cell death detection ELISA, and the gene expression was analyzed by real time RT-PCR.

Results: IL-24 transduction suppressed the growth of prostate cancer and induced tumor cell apoptosis. In addition, up-regulation of epithelial markers and down-regulation of mesenchymal markers were noted, suggesting that tumor aggressiveness was reduced.

Conclusion: Introduction of IL-24 displays antitumor activity both by induction of apoptosis and regulation of anchorage dependence.

Keywords: IL-24; anchorage dependence; prostate cancer; stable retroviral transfection.

MeSH terms

  • Apoptosis
  • Cell Proliferation
  • Humans
  • Interleukins / genetics*
  • Male
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / pathology*
  • Transduction, Genetic

Substances

  • Interleukins
  • interleukin-24