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Expression of cell cycle regulator cdk2ap1 suppresses tumor cell phenotype by non-cell-autonomous mechanisms

Olga Zolochevska1, Marxa L Figueiredo

  • 1Department of Comparative Biomedical Sciences, Louisiana State University, Baton Rouge, 70803, United States.

Oral Oncology
|June 12, 2009
PubMed

Insights

Expressing cdk2ap1 in cancer cells or surrounding fibroblasts reduces squamous cell carcinoma (SCC) growth and invasion. This study highlights cdk2ap1

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Squamous cell carcinoma (SCC) growth is influenced by interactions between cancer cells and the tumor microenvironment.
  • The cell cycle regulator cdk2ap1's role in SCC tumorigenesis is not fully understood.

Purpose of the Study:

  • To investigate the effect of cdk2ap1 expression in epithelial and stromal cells on SCC growth.
  • To elucidate the mechanisms by which cdk2ap1 influences tumor progression.

Main Methods:

  • In vitro phenotype assays and quantitative real-time PCR were used to assess gene expression changes.
  • In vivo studies utilized a novel three-way xenograft animal model for molecular imaging.
  • cdk2ap1 was expressed in either epithelial or stromal cell compartments.

Main Results:

  • Expression of cdk2ap1 in either cell type significantly reduced SCC tumor growth and invasion.
  • cdk2ap1 altered the expression of genes involved in cell cycle, adhesion, invasion, angiogenesis, and apoptosis.
  • Non-cell-autonomous effects of cdk2ap1 on tumor microenvironment interactions were observed.

Conclusions:

  • cdk2ap1 acts as a tumor suppressor by modulating cell-autonomous and non-cell-autonomous pathways.
  • Targeting cdk2ap1 interactions within the tumor microenvironment offers a novel therapeutic strategy for SCC.
  • Minimizing cancer cell-fibroblast interactions through cdk2ap1 expression can inhibit SCC progression.

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