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Regulation of FGF-2 by an endogenous antisense RNA: effects on cell adhesion and cell-cycle progression

Leigh-Ann MacFarlane1, Paul R Murphy

  • 1Faculty of Medicine, Department of Physiology & Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada.

Molecular Carcinogenesis
|October 15, 2010
PubMed

Insights

Fibroblast growth factor antisense RNA (FGF-AS) and fibroblast growth factor-2 (FGF-2) regulate cancer cell adhesion, cell-cycle progression, and invasion. FGF-AS expression correlates with better outcomes in certain cancers.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Fibroblast growth factor (FGF-2) and its antisense RNA (FGF-AS) are linked to cancer progression and patient outcomes.
  • Previous studies indicated FGF-AS expression correlates with reduced tumor recurrence and improved survival in esophageal adenocarcinoma.
  • The interplay between FGF-2 and FGF-AS in cancer biology requires further elucidation.

Purpose of the Study:

  • To investigate the reciprocal effects of FGF-AS and FGF-2 on gene expression and cellular behavior.
  • To determine the impact of siRNA-mediated knockdown of FGF-AS and FGF-2 on cell adhesion, cell-cycle progression, and invasion.
  • To understand the regulatory mechanisms underlying the protective role of FGF-AS in FGF-2-dependent cancers.

Main Methods:

  • Utilized siRNA to knockdown FGF-AS and FGF-2 expression in cancer cells.
  • Assessed changes in complementary transcript and protein levels.
  • Performed cell-substratum adhesion assays, microarray analysis, RT-PCR, and cell-cycle analysis.
  • Quantified invasion activity.

Main Results:

  • siRNA knockdown of FGF-AS or FGF-2 led to upregulation of the complementary transcript and protein.
  • FGF-AS knockdown significantly increased cell-substratum adhesion and altered expression of adhesion molecules.
  • Antithetical effects on cell-cycle-related genes (SKP2, SESTRIN-3, EIF4BP2, CDC27, P190RhoGAP) were observed between FGF-AS and FGF-2 knockdown.
  • Both FGF-AS and FGF-2 influence G1 and G2 cell-cycle transitions, affecting proliferation and apoptosis.
  • FGF-AS knockdown resulted in a significant increase in invasion activity.

Conclusions:

  • Regulatory interactions between FGF-AS and FGF-2 control cell adhesion, cell-cycle progression, and invasion.
  • These findings provide a molecular basis for the observed protective effects of FGF-AS in FGF-2-dependent cancers.
  • FGF-AS may serve as a potential therapeutic target or biomarker in specific cancer types.

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