Disruption of transforming growth factor-beta signaling through beta-spectrin ELF leads to hepatocellular cancer through cyclin D1 activation

Oncogene. 2007 Nov 1;26(50):7103-10. doi: 10.1038/sj.onc.1210513. Epub 2007 Jun 4.

Abstract

Transforming growth factor-beta (TGF-beta) signaling members, TGF-beta receptor type II (TBRII), Smad2, Smad4 and Smad adaptor, embryonic liver fodrin (ELF), are prominent tumor suppressors in gastrointestinal cancers. Here, we show that 40% of elf(+/-) mice spontaneously develop hepatocellular cancer (HCC) with markedly increased cyclin D1, cyclin-dependent kinase 4 (Cdk4), c-Myc and MDM2 expression. Reduced ELF but not TBRII, or Smad4 was observed in 8 of 9 human HCCs (P<0.017). ELF and TBRII are also markedly decreased in human HCC cell lines SNU-398 and SNU-475. Restoration of ELF and TBRII in SNU-398 cells markedly decreases cyclin D1 as well as hyperphosphorylated-retinoblastoma (hyperphosphorylated-pRb). Thus, we show that TGF-beta signaling and Smad adaptor ELF suppress human hepatocarcinogenesis, potentially through cyclin D1 deregulation. Loss of ELF could serve as a primary event in progression toward a fully transformed phenotype and could hold promise for new therapeutic approaches in human HCCs.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Carcinoma, Hepatocellular / etiology*
  • Carcinoma, Hepatocellular / metabolism*
  • Carrier Proteins / genetics
  • Carrier Proteins / physiology*
  • Cell Line, Tumor
  • Cyclin D
  • Cyclins / antagonists & inhibitors
  • Cyclins / metabolism*
  • Humans
  • Liver Neoplasms, Experimental / etiology*
  • Liver Neoplasms, Experimental / metabolism
  • Mice
  • Mice, Knockout
  • Microfilament Proteins / deficiency
  • Microfilament Proteins / genetics
  • Microfilament Proteins / physiology*
  • Phosphorylation
  • Receptors, Transforming Growth Factor beta / metabolism
  • Retinoblastoma / metabolism
  • Signal Transduction / genetics
  • Signal Transduction / physiology*
  • Spectrin / deficiency
  • Spectrin / genetics
  • Spectrin / physiology*
  • Transforming Growth Factor beta2 / antagonists & inhibitors*
  • Transforming Growth Factor beta2 / metabolism
  • Transforming Growth Factor beta2 / physiology
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / physiology

Substances

  • Carrier Proteins
  • Cyclin D
  • Cyclins
  • Microfilament Proteins
  • Receptors, Transforming Growth Factor beta
  • Transforming Growth Factor beta2
  • Tumor Suppressor Proteins
  • fodrin
  • Spectrin