Emerging role of miR-106b-25/miR-17-92 clusters in the control of transforming growth factor beta signaling

Cancer Res. 2008 Oct 15;68(20):8191-4. doi: 10.1158/0008-5472.CAN-08-1768.

Abstract

Inactivation of the transforming growth factor beta (TGFbeta) tumor suppressor pathway is a main step in the development of a variety of human tumors. The miR-106b-25 and miR-17-92 clusters are emerging as key modulators of TGFbeta signaling in gastrointestinal and other tumors, interfering with cell cycle arrest and apoptosis when overexpressed in cancer cells. Genetic ablation of these microRNAs (miRNAs) reveals their physiologic role in the control of liver and central nervous system apoptosis, supporting the notion that miRNA-based homeostatic mechanisms can be usurped by cancer cells to resist TGFbeta tumor suppression.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Apoptosis Regulatory Proteins / physiology
  • Bcl-2-Like Protein 11
  • Cell Cycle Proteins / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / physiology
  • DNA-Binding Proteins / genetics
  • E2F1 Transcription Factor / physiology
  • Genes, myc
  • Humans
  • Membrane Proteins / physiology
  • MicroRNAs / physiology*
  • Minichromosome Maintenance Complex Component 7
  • Multigene Family
  • Neoplasms / etiology
  • Nuclear Proteins / genetics
  • Proto-Oncogene Proteins / physiology
  • RNA Interference
  • Signal Transduction / physiology*
  • Transforming Growth Factor beta / physiology*
  • Tumor Suppressor Proteins / physiology*

Substances

  • Apoptosis Regulatory Proteins
  • BCL2L11 protein, human
  • Bcl-2-Like Protein 11
  • CDKN1A protein, human
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • DNA-Binding Proteins
  • E2F1 Transcription Factor
  • E2F1 protein, human
  • Membrane Proteins
  • MicroRNAs
  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Transforming Growth Factor beta
  • Tumor Suppressor Proteins
  • MCM7 protein, human
  • Minichromosome Maintenance Complex Component 7