MELK is an oncogenic kinase essential for mitotic progression in basal-like breast cancer cells

Elife. 2014 May 20:3:e01763. doi: 10.7554/eLife.01763.

Abstract

Despite marked advances in breast cancer therapy, basal-like breast cancer (BBC), an aggressive subtype of breast cancer usually lacking estrogen and progesterone receptors, remains difficult to treat. In this study, we report the identification of MELK as a novel oncogenic kinase from an in vivo tumorigenesis screen using a kinome-wide open reading frames (ORFs) library. Analysis of clinical data reveals a high level of MELK overexpression in BBC, a feature that is largely dependent on FoxM1, a master mitotic transcription factor that is also found to be highly overexpressed in BBC. Ablation of MELK selectively impairs proliferation of basal-like, but not luminal breast cancer cells both in vitro and in vivo. Mechanistically, depletion of MELK in BBC cells induces caspase-dependent cell death, preceded by defective mitosis. Finally, we find that Melk is not required for mouse development and physiology. Together, these data indicate that MELK is a normally non-essential kinase, but is critical for BBC and thus represents a promising selective therapeutic target for the most aggressive subtype of breast cancer.DOI: http://dx.doi.org/10.7554/eLife.01763.001.

Keywords: FoxM1; MELK; basal-like breast cancer; targeted therapy; triple-negative breast cancer.

Publication types

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

MeSH terms

  • Animals
  • Breast Neoplasms / pathology*
  • Cell Proliferation*
  • Disease Models, Animal
  • Epithelial Cells / physiology*
  • Female
  • Forkhead Box Protein M1
  • Forkhead Transcription Factors / metabolism
  • Gene Expression Profiling
  • Gene Knockout Techniques
  • Humans
  • Mice
  • Mitosis*
  • Protein Serine-Threonine Kinases / metabolism*
  • Stem Cells
  • Transplantation, Heterologous

Substances

  • FOXM1 protein, human
  • Forkhead Box Protein M1
  • Forkhead Transcription Factors
  • MELK protein, human
  • Protein Serine-Threonine Kinases