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

Olga Cain, Marxa L. Figueiredo

Research output: Contribution to journalArticle

10 Citations (Scopus)

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)
JournalOral Oncology
Volume45
Issue number9
DOIs
StatePublished - Sep 2009
Externally publishedYes

Fingerprint

Cell Cycle
Tumor Suppressor Genes
Phenotype
Growth
Neoplasms
Molecular Imaging
Tumor Microenvironment
Stromal Cells
Heterografts
Cell Adhesion
Real-Time Polymerase Chain Reaction
Carcinogenesis
Animal Models
Fibroblasts
Epithelial Cells
Gene Expression
In Vitro Techniques

Keywords

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

ASJC Scopus subject areas

  • Oncology
  • Oral Surgery
  • Cancer Research

Cite this

Expression of cell cycle regulator cdk2ap1 suppresses tumor cell phenotype by non-cell-autonomous mechanisms. / Cain, Olga; Figueiredo, Marxa L.

In: Oral Oncology, Vol. 45, No. 9, 09.2009.

Research output: Contribution to journalArticle

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