Negative Regulatory Loop between Microphthalmia-Associated Transcription Factor (MITF) and Notch Signaling

Int J Mol Sci. 2019 Jan 29;20(3):576. doi: 10.3390/ijms20030576.

Abstract

Melanoma, a melanocyte-origin neoplasm, is a highly metastatic and treatment-resistance cancer. While it is well established that notch signaling activation promotes melanoma progression, little is known about the reciprocal interactions between Notch signaling and melanoma-specific pathways. Here we reveal a negative regulatory loop between Notch signaling and microphthalmia-associated transcription factor (MITF), the central regulator of melanoma progression and the driver of melanoma plasticity. We further demonstrate that Notch signaling activation, in addition to the known competition-based repression mechanism of MITF transcriptional activity, inhibits the transcription of MITF, leading to a decrease in MITF expression. We also found that MITF binds to the promoter of the gene encoding the master regulator of Notch signaling, recombination signal binding protein J kappa (RBPJK), leading to its upregulation. Our findings suggest that, once activated, Notch signaling represses MITF signaling to maintain the melanoma invasiveness and metastatic phenotype.

Keywords: MITF; melanoma; notch signaling.

MeSH terms

  • Animals
  • CHO Cells
  • Cell Line, Tumor
  • Chromatin Immunoprecipitation
  • Cricetulus
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Melanocytes / metabolism
  • Melanoma / metabolism
  • Melanoma, Cutaneous Malignant
  • Microphthalmia-Associated Transcription Factor / metabolism*
  • Promoter Regions, Genetic / genetics
  • Receptors, Notch / metabolism
  • Signal Transduction
  • Skin Neoplasms / metabolism

Substances

  • Microphthalmia-Associated Transcription Factor
  • Receptors, Notch