Positive auto-regulation of MYCN in human neuroblastoma

Biochem Biophys Res Commun. 2009 Dec 4;390(1):21-6. doi: 10.1016/j.bbrc.2009.09.044. Epub 2009 Sep 18.

Abstract

MYCN oncogene is one of the most important regulators affecting the prognosis of neuroblastoma and is frequently amplified in the high-risk subsets. Despite its clinical significance, it remains unclear how the MYCN expression is regulated in human neuroblastomas. Here, we found the presence of a positive auto-regulatory mechanism of MYCN. Enforced expression of MYCN induced endogenous MYCN mRNA expression in SK-N-AS neuroblastoma cells with a single copy of MYCN gene. Luciferase reporter assay revealed that MYCN protein activates its own promoter activity in a dose-dependent manner and the downstream region relative to the transcription start sites is responsible for the activation. Furthermore, ChIP analysis showed that MYCN is directly recruited onto the intron 1 region of MYCN gene which contains two putative E-box sites. Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Collectively, our present results suggest that MYCN contributes to its own expression by forming a positive auto-regulatory loop in neuroblastoma cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Chromatin Immunoprecipitation
  • E-Box Elements
  • Gene Expression Regulation*
  • Genome, Human / drug effects
  • Homeostasis
  • Humans
  • N-Myc Proto-Oncogene Protein
  • Neuroblastoma / metabolism*
  • Neurogenesis / genetics*
  • Neurons / cytology
  • Neurons / physiology
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism*
  • Oncogene Proteins / genetics*
  • Oncogene Proteins / metabolism*
  • Promoter Regions, Genetic / drug effects
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Tretinoin / pharmacology

Substances

  • MYCN protein, human
  • N-Myc Proto-Oncogene Protein
  • Nuclear Proteins
  • Oncogene Proteins
  • RNA, Messenger
  • Tretinoin