Related Experiment Videos

Cten, a COOH-terminal tensin-like protein with prostate restricted expression, is down-regulated in prostate cancer

Su Hao Lo1, Tung Bin Lo

  • 1Center for Tissue Regeneration and Repair, Department of Orthopaedic Surgery, The University of California-Davis, Sacramento, California 95817, USA. shlo@ucdavis.edu

Cancer Research
|August 3, 2002
PubMed

Insights

A new gene family member, cten, binds to focal adhesions and is expressed in the prostate and placenta. Its down-regulation in prostate cancer suggests a role in preventing tumor formation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Tensin proteins are signaling molecules that bind actin filaments and localize to focal adhesions.
  • Tensin represents a newly discovered gene family with diverse tissue expression.
  • Focal adhesions are critical sites for cell adhesion and signal transduction.

Purpose of the Study:

  • To identify and characterize a novel COOH-terminal tensin-like molecule, designated cten.
  • To investigate the evolutionary relationship of cten to the tensin gene family.
  • To determine the tissue-specific expression and potential role of cten in prostate cancer.

Main Methods:

  • Human cten cDNA sequencing and analysis.
  • Genomic structure analysis to infer evolutionary relationships.
  • Northern blot analysis for tissue expression profiling.
  • Examination of cten expression in prostate cancer cell lines.

Main Results:

  • Human cten encodes a 715 amino acid protein with Src homology 2 and phosphotyrosine-binding domains, similar to tensins.
  • cten lacks an actin-binding domain but localizes to focal adhesions.
  • cten expression is predominantly restricted to the prostate and placenta.
  • cten is significantly down-regulated in prostate cancer samples.

Conclusions:

  • cten has evolved as a focal adhesion protein mediating signal transduction via its SH2 and PTB domains.
  • Evolutionary divergence has resulted in cten losing actin-binding but gaining specific expression in prostate and placenta.
  • The down-regulation of cten in prostate cancer suggests its potential role as a tumor suppressor, possibly preventing tumor formation.

Related Concept Videos