Transient reduction of PTI-1 expression by short interfering RNAs inhibits the growth of human prostate cancer cell lines

Tohoku J Exp Med. 2006 Jun;209(2):141-8. doi: 10.1620/tjem.209.141.

Abstract

The prostate tumor-inducing gene 1 (PTI-1) was originally identified by differential ribonucleic acid (RNA) display in human prostate carcinoma. PTI-1 is expressed in human prostate carcinoma but not in benign prostate hypertrophy or normal prostate tissue. PTI-1 may be a member of oncogenes that could affect protein translation and contribute to carcinoma development in human prostate. To investigate the role of PTI-1 in human prostate carcinoma, we constructed three different short interfering RNA (siRNA) vectors (pSilencer3.1-neo-Yu Lei [YL]1-2, -YL3-4 and -YL5-6), each of which was transfected into DU145 and PC3 human prostate cancer cell lines. Among these siRNAs, only pSilencer3.1-neo-YL1-2 could almost completely block the expression of PTI-1 in these two cell lines. The growth of the cell lines was then evaluated after transfection. The proliferation rate was retarded in DU145 and PC3 cells transfected with pSilencer3.1-neo-YL1-2, compared with the cells transfected with a control vector; namely, about 88.6% of DU145 and 80.2% of PC3 cancer cells were blocked at the G1 phase when transfected with pSilencer3.1-neo-YL1-2, compared to 62.0% in DU145 cells and 51.7% in PC3 cells, transfected with the control vector. Moreover, 68.3% of DU145 cells and 72.3% of PC3 cells were induced into apoptosis, while in control transfection, the population was 26.6% in DU145 cells and 28.4% in PC3 cells. These results indicate that blocking PTI-1 expression can inhibit the growth of certain prostate cancer cell lines. We suggest that PTI-1 may serve as a target for the gene-based therapy of human prostate carcinoma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / pathology*
  • Adenocarcinoma / prevention & control
  • Cell Line, Tumor
  • Cell Proliferation
  • DNA Primers / genetics
  • Gene Expression Regulation, Neoplastic*
  • Gene Silencing
  • Genetic Therapy / methods
  • Humans
  • Male
  • Oncogene Proteins / antagonists & inhibitors*
  • Oncogene Proteins / genetics
  • Peptide Elongation Factor 1 / antagonists & inhibitors*
  • Peptide Elongation Factor 1 / genetics
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / pathology*
  • Prostatic Neoplasms / prevention & control
  • RNA Interference*
  • RNA, Small Interfering / pharmacology*
  • Transfection

Substances

  • DNA Primers
  • EEF1A1 protein, human
  • Oncogene Proteins
  • Peptide Elongation Factor 1
  • RNA, Small Interfering