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

Olga Zolochevska, Marxa L. Figueiredo

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

We evaluated the effect of expressing the cell cycle regulator cdk2ap1 in epithelial or stromal cell compartments to reduce SCC growth in vitro and in vivo. Cell-autonomous and/or non-cell-autonomous expression of cdk2ap1 reduced tumor growth and invasion and altered cell cycle, adhesion, invasion, angiogenesis, and apoptotic gene expression, as assessed by several in vitro phenotype assays, quantitative real-time PCR, and in vivo molecular imaging using a novel three-way xenograft animal model. Our findings suggest that the interactions between cancer cells and fibroblasts that promote abnormal growth can be minimized by expressing cdk2ap1, supporting a novel concept by which tumor/growth suppressor genes can impact tumorigenesis phenotypes from non-cell-autonomous interactions within the tumor microenvironment.

Original languageEnglish (US)
Pages (from-to)e106-e112
JournalOral Oncology
Volume45
Issue number9
DOIs
StatePublished - Sep 2009

Keywords

  • Non-cell-autonomous
  • Oral cancer
  • Squamous cell carcinoma
  • Stromal-epithelial interactions
  • Tumor suppression
  • cdk2ap1

ASJC Scopus subject areas

  • Oral Surgery
  • Oncology
  • Cancer Research

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