ST7-mediated suppression of tumorigenicity of prostate cancer cells is characterized by remodeling of the extracellular matrix

Oncogene. 2006 Jun 29;25(28):3924-33. doi: 10.1038/sj.onc.1209418. Epub 2006 Feb 13.

Abstract

Multiple lines of evidence have provided compelling evidence for the existence of a tumor suppressor gene (TSG) on chromosome 7q31.1. ST7 may be the target of this genetic instability but its designation as a TSG is controversial. In this study, we show that, functionally, ST7 behaves as a tumor suppressor in human cancer. ST7 suppressed growth of PC-3 prostate cancer cells inoculated subcutaneously into severe combined immunodeficient mice, and increased the latency of tumor detection from 13 days in control tumors to 23 days. Re-expression of ST7 was also associated with suppression of colony formation under anchorage-independent conditions in MDA-MB-231 breast cancer cells and ST7 mRNA expression was downregulated in 44% of primary breast cancers. Expression profiling of PC-3 cells revealed that ST7 predominantly induces changes in genes involved in re-modeling the extracellular matrix such as SPARC, IGFBP5 and several matrix metalloproteinases. These data indicate that ST7 may mediate tumor suppression through modification of the tumor microenvironment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Blotting, Northern
  • Blotting, Western
  • Breast Neoplasms / genetics
  • Cell Line, Tumor
  • Cell Proliferation
  • DNA Primers
  • Gene Expression Profiling
  • Humans
  • Male
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / pathology*
  • Transcription, Genetic
  • Tumor Suppressor Proteins / physiology*

Substances

  • DNA Primers
  • ST7 protein, human
  • Tumor Suppressor Proteins