MicroRNA-135b promotes cancer progression by acting as a downstream effector of oncogenic pathways in colon cancer

Cancer Cell. 2014 Apr 14;25(4):469-83. doi: 10.1016/j.ccr.2014.03.006.

Abstract

MicroRNA deregulation is frequent in human colorectal cancers (CRCs), but little is known as to whether it represents a bystander event or actually drives tumor progression in vivo. We show that miR-135b overexpression is triggered in mice and humans by APC loss, PTEN/PI3K pathway deregulation, and SRC overexpression and promotes tumor transformation and progression. We show that miR-135b upregulation is common in sporadic and inflammatory bowel disease-associated human CRCs and correlates with tumor stage and poor clinical outcome. Inhibition of miR-135b in CRC mouse models reduces tumor growth by controlling genes involved in proliferation, invasion, and apoptosis. We identify miR-135b as a key downsteam effector of oncogenic pathways and a potential target for CRC treatment.

Publication types

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

MeSH terms

  • Animals
  • Cell Growth Processes / genetics
  • Cell Line, Tumor
  • Colonic Neoplasms / genetics*
  • Colonic Neoplasms / metabolism
  • Colonic Neoplasms / pathology
  • Disease Models, Animal
  • Disease Progression
  • Heterografts
  • Humans
  • Immunohistochemistry
  • Mice
  • Mice, Inbred C57BL
  • Mice, Nude
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Transfection

Substances

  • MIRN135 microRNA, human
  • MicroRNAs

Associated data

  • GEO/GSE54163
  • GEO/GSE54177