Overexpression of high molecular weight FGF-2 forms inhibits glioma growth by acting on cell-cycle progression and protein translation

Exp Cell Res. 2008 Dec 10;314(20):3701-11. doi: 10.1016/j.yexcr.2008.09.022. Epub 2008 Oct 7.

Abstract

In order to clarify the role of HMW FGF-2 in glioma development and angiogenesis, we over-expressed different human FGF-2 isoforms in C6 rat glioma cell line using a tetracycline-regulated expression system. Phenotypic modifications were analyzed in vitro and compared to untransfected cells or to cells over-expressing 18 kDa FGF-2 or all FGF-2 isoforms. In particular, we demonstrate that HMW FGF-2 has unique features in inhibiting glioma cell proliferation. HMW FGF-2 expressing cells showed a cell-cycle arrest at the G2M, demonstrating a role of HMW FGF-2 in controlling the entry in mitosis. Moreover, hydroxyurea was ineffective in blocking cells at the G1S boundary when HMW FGF-2 was expressed. We also show that the HMW FGF-2 isoforms inhibit 4E-BP1 phosphorylation at critical sites restoring the translation inhibitory activity of 4E-BP1. In vivo, inhibition of tumor growth was observed when cells expressed HMW FGF-2. This indicates that HMW FGF-2 inhibits tumor growth in glioma cells by acting on cell-cycle progression and protein translation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle / genetics*
  • Cell Cycle / physiology
  • Cell Line, Tumor
  • Cell Proliferation*
  • Down-Regulation
  • Fibroblast Growth Factor 2 / genetics*
  • Glioma / genetics*
  • Glioma / metabolism
  • Glioma / pathology
  • Humans
  • Mice
  • Mice, SCID
  • Molecular Weight
  • Protein Biosynthesis / genetics*
  • Protein Isoforms / genetics
  • Rats
  • Transfection
  • Tumor Burden / genetics
  • Xenograft Model Antitumor Assays

Substances

  • Protein Isoforms
  • Fibroblast Growth Factor 2