[c-MYC-mediated regulations in colorectal cancer]

A Menssen1

  • 1Deutsches Konsortium für Translationale Krebsforschung, Pathologisches Institut, Ludwig-Maximilians-Universität München, Thalkirchnerstr. 36, 80337, München, Deutschland, Antje.Menssen@med.uni-muenchen.de.

Der Pathologe
|November 8, 2013
PubMed

Insights

The oncogenic transcription factor c-MYC drives tumor properties like immortalization. Researchers identified c-MYC target genes, including SIRT1, that mediate these effects in human cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Context:

  • The transcription factor c-MYC is frequently deregulated in human tumors.
  • Deregulated c-MYC contributes to key cancer hallmarks such as cell cycle progression, transformation, genomic instability, and immortalization.
  • Identifying c-MYC target genes is crucial for understanding its oncogenic mechanisms.

Purpose:

  • To identify novel c-MYC target genes using genome-wide approaches.
  • To characterize the role of specific c-MYC target genes in mediating c-MYC-induced genomic instability and immortalization.
  • To validate the relevance of identified c-MYC target genes in human tumorigenesis.

Summary:

  • Genome-wide analyses identified numerous c-MYC target genes.
  • The protein deacetylase SIRT1 was identified as a key mediator of c-MYC-induced immortalization.
  • In situ analyses of colorectal cancer specimens confirmed c-MYC's regulatory role in these target genes within human tumors.

Impact:

  • This study elucidates critical downstream effectors of c-MYC in cancer development.
  • Findings highlight potential therapeutic targets for cancers driven by c-MYC.
  • The identified target genes, including SIRT1, are implicated in human tumorigenesis, particularly colorectal cancer.

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