Lack of correlation between the decreased expression of cell surface LETS protein and tumorigenicity in human cell

Cell
|December 1, 1978
PubMed

Insights

This study found no direct link between tumorigenicity and reduced expression of large external transformation-sensitive glycoprotein (LETS). Altered LETS expression alone does not guarantee tumor formation, suggesting separate controls for cell transformation and tumorigenicity.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • The large external transformation-sensitive glycoprotein (LETS) is a cell surface protein implicated in cell adhesion and morphology.
  • Loss of LETS expression has been hypothesized to correlate with cellular transformation and tumorigenicity.

Purpose of the Study:

  • To investigate the correlation between tumorigenicity and the expression levels of the large external transformation-sensitive glycoprotein (LETS) in human cell hybrids.
  • To determine if alterations in LETS protein expression are a sufficient condition for the development of tumors.

Main Methods:

  • Analysis of LETS protein expression using immunofluorescent staining and gel electrophoresis of iodinated cell surface proteins.
  • Assaying the tumorigenicity of cell lines in nude mice models.
  • Comparison of LETS expression in normal, transformed, and tumorigenic cell lines and their hybrids.

Main Results:

  • No direct correlation was observed between tumorigenicity and decreased expression of LETS protein across a broad spectrum of cell lines.
  • Transformed, nontumorigenic hybrids showed altered LETS expression (decreased complexity and content) alongside other transformed phenotypes.
  • Tumorigenic hybrids exhibited variable LETS protein levels, with some maintaining relatively high expression compared to nontumorigenic counterparts.

Conclusions:

  • Alterations in LETS protein expression, individually or with other transformation properties, are not sufficient to induce tumorigenicity.
  • The findings support a model where the transformed phenotype and tumorigenic potential are regulated independently.