Roles of 14-3-3η in mitotic progression and its potential use as a therapeutic target for cancers

Oncogene. 2013 Mar 21;32(12):1560-9. doi: 10.1038/onc.2012.170. Epub 2012 May 7.

Abstract

14-3-3 proteins are involved in several cellular processes, including the G1/S and G2/M cell cycle transitions. However, their roles during mitosis are not well understood. Here, we showed that depletion of 14-3-3η, a 14-3-3 protein isoform, enhanced mitotic cell death, resulting in sensitization to microtubule inhibitors and inhibition of aneuploidy formation. The enhanced mitotic cell death by depletion of 14-3-3η appeared to be both caspase-dependent and independent. Furthermore, enhanced mitotic cell death and a reduction in aneuploidy following 14-3-3η depletion were independent of the mitotic checkpoint, which is thought to be the primary signaling event in the regulation of the cell death induced by microtubule inhibitors. When 14-3-3η depletion was combined with microtubule inhibitors in HCT116 and U87MG cells, it sensitized both cancer cell lines to microtubule inhibitors. These results collectively suggest that 14-3-3η may be required for mitotic progression and may be considered as a novel anti-cancer strategy in combination with microtubule inhibitors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 14-3-3 Proteins / antagonists & inhibitors
  • 14-3-3 Proteins / physiology*
  • Aneuploidy
  • Apoptosis / drug effects
  • Caspase 9 / physiology
  • Cell Division
  • Forkhead Box Protein O3
  • Forkhead Transcription Factors / physiology
  • G2 Phase
  • HeLa Cells
  • Humans
  • Microtubules / drug effects
  • Mitosis*
  • Neoplasms / drug therapy*
  • Neoplasms / pathology
  • Nocodazole / pharmacology

Substances

  • 14-3-3 Proteins
  • FOXO3 protein, human
  • Forkhead Box Protein O3
  • Forkhead Transcription Factors
  • YWHAH protein, human
  • Caspase 9
  • Nocodazole