PRL-3 phosphatase is implicated in ovarian cancer growth

Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):6835-9. doi: 10.1158/1078-0432.CCR-04-2357.

Abstract

Purpose: The PRL-3 phosphatase has been found expressed at higher levels in metastasis than in primary tumors of patients with colorectal cancer. In the present study, we evaluated the expression of PRL-3 in ovarian cancer tissue and its role in ovarian cancer cell growth.

Experimental design: PRL-3 phosphatase expression was evaluated in 84 ovarian tumor samples. PRL-3 expression has been knocked down using specific small interfering RNAs to determine its role in ovarian cancer cell growth in vitro.

Results: In ovarian cancers, PRL-3 expression correlates with disease progression, being higher in advanced (stage III) than in early (stage I) tumors. In situ measurements of PRL-3 expression showed that it was confined to the epithelial neoplastic cells. The molecular mechanism underlying PRL-3 overexpression in ovarian cancers is independent from amplification of the corresponding genomic locus. Ovarian cancer cells growing in culture have high levels of expression of this phosphatase. PRL-3-specific knockdown using small interfering RNA severely impaired the growth of cells without affecting the expression of the closely related homologue PRL-1. Intriguingly, the growth of human colon carcinoma cells expressing lower levels of the PRL-3 was not affected by the PRL-3 knockdown.

Conclusions: Altogether, these results show that PRL-3 expression is associated with ovarian cancer progression and point to a key role for this phosphatase in the control of ovarian cancer cells growth. This strongly suggests that PRL-3 should be considered as a target for the discovery of new anticancer agents to be tested against this malignancy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Proliferation
  • Disease Progression
  • Epithelial Cells / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Immediate-Early Proteins / physiology*
  • In Situ Hybridization
  • Neoplasm Proteins / physiology*
  • Ovarian Neoplasms / enzymology*
  • Protein Tyrosine Phosphatases / physiology*
  • RNA / chemistry
  • RNA, Messenger / metabolism
  • RNA, Small Interfering / metabolism
  • Time Factors

Substances

  • Antineoplastic Agents
  • Immediate-Early Proteins
  • Neoplasm Proteins
  • RNA, Messenger
  • RNA, Small Interfering
  • RNA
  • PTP4A3 protein, human
  • Protein Tyrosine Phosphatases