Post-transcriptional and post-translational regulation of PTEN by transforming growth factor-beta1

J Cell Biochem. 2009 Apr 15;106(6):1102-12. doi: 10.1002/jcb.22100.

Abstract

PTEN is a critical tumor suppressor gene mutated frequently in various human cancers. Previous studies have showed that PTEN mRNA expression is down-regulated by TGF-beta1 in various cell lines. In present study, we have found that TGF-beta1 down-regulates PTEN mRNA and protein expression in a dose- and time-dependent manner in hepatocarcinoma cell line SMMC-7721. Based on the PTEN promoter dual-luciferase report assay, we have found that PTEN transcription is not affected by TGF-beta1. By using transcriptional inhibitor actinomycin D (Act D), the turnover rate of PTEN transcripts appeared to be accelerated during TGF-beta1 stimulation, which indicated that down-regulation of PTEN by TGF-beta1 was post-transcriptional. What interested us was that transfection of PTEN coding sequence increased TGF-beta1-induced degradation of PTEN mRNA, suggesting that PTEN coding region was account for TGF-beta1-mediated down-regulation of PTEN. In addition, TGF-beta1 down-regulated PTEN expression was blocked by the TbetaIR inhibitor SB431542 and the p38 inhibitor SB203580, suggesting Smad and p38 MAPK signal pathways played crucial roles in PTEN down-regulation via TGF-beta1 stimulation. In this study, we also found TGF-beta1 accelerated down-regulation of PTEN through the ubiquitin-proteasome pathway. Collectively, our data clearly demonstrated that TGF-beta1-mediated down-regulation of PTEN was post-transcriptional and post-translational, depending on its coding sequence, Smad and p38-MAPK signal pathways were involved in this down-regulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carcinoma, Hepatocellular
  • Cell Line, Tumor
  • Gene Expression Regulation, Enzymologic*
  • Humans
  • Liver Neoplasms
  • PTEN Phosphohydrolase / genetics*
  • PTEN Phosphohydrolase / metabolism
  • Promoter Regions, Genetic
  • Protein Processing, Post-Translational
  • RNA Stability
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / metabolism
  • Signal Transduction / physiology
  • Smad Proteins / genetics
  • Smad Proteins / metabolism
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism*
  • p38 Mitogen-Activated Protein Kinases / genetics
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • RNA, Messenger
  • Recombinant Fusion Proteins
  • Smad Proteins
  • Transforming Growth Factor beta1
  • p38 Mitogen-Activated Protein Kinases
  • PTEN Phosphohydrolase
  • PTEN protein, human