AURKA Overexpression Is Driven by FOXM1 and MAPK/ERK Activation in Melanoma Cells Harboring BRAF or NRAS Mutations: Impact on Melanoma Prognosis and Therapy

J Invest Dermatol. 2017 Jun;137(6):1297-1310. doi: 10.1016/j.jid.2017.01.021. Epub 2017 Feb 7.

Abstract

The cell cycle-related genes AURKA and FOXM1 are overexpressed in melanoma. We show here that AURKA overexpression is associated with poor prognosis in three independent cohorts of melanoma patients and correlates with the presence of genomic amplification of AURKA locus and BRAFV600E mutation. AURKA overexpression may also be driven by increased promoter activation through elements such as ETS and FOXM1 found within the 5' proximal promoter region. Activated MAPK/ERK signaling pathway mediates robust AURKA promoter activation, thereby knockdown of BRAFV600E and ERK inhibition results in reduced AURKA transcription and expression. We show a positive correlation between FOXM1 and AURKA expression in three independent cohorts of melanoma patients. FOXM1 silencing decreases expression of AURKA and late cell cycle genes in melanoma cells. We further found that FOXM1 expression levels are significantly higher in tumors carrying the BRAFV600E mutation compared with the wild-type BRAF (BRAFwt). Accordingly, the knockdown of BRAFV600E also reduces the expression of FOXM1 in BRAFV600E cells. Moreover, Aurora kinase A and FOXM1 inhibition by either genetic knockdown or pharmacologic inhibitors impair melanoma growth and survival both in culture and in vivo, underscoring their therapeutic value for melanoma patients who fail to benefit from BRAF/MEK signaling inhibition.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aspartate-tRNA Ligase / genetics*
  • Aurora Kinase A / genetics*
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Cell Survival / genetics
  • Forkhead Box Protein M1 / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Melanoma / genetics
  • Melanoma / pathology
  • Melanoma / therapy
  • Mice
  • Mitogen-Activated Protein Kinase Kinases / metabolism
  • Mutation*
  • Proto-Oncogene Proteins B-raf / genetics
  • RNA, Transfer, Amino Acyl / genetics*
  • Sensitivity and Specificity
  • Signal Transduction
  • Skin Neoplasms / genetics
  • Skin Neoplasms / pathology
  • Skin Neoplasms / therapy
  • Xenograft Model Antitumor Assays

Substances

  • FOXM1 protein, human
  • Forkhead Box Protein M1
  • RNA, Transfer, Amino Acyl
  • AURKA protein, human
  • Aurora Kinase A
  • Proto-Oncogene Proteins B-raf
  • Mitogen-Activated Protein Kinase Kinases
  • Aspartate-tRNA Ligase
  • asparaginyl-tRNA synthetase