Deleted in Colorectal Cancer (DCC) pathfinding

Axon guidance gene finally turned tumor suppressor

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Loss of heterozygosity (LOH) at human chromosome 18q, which includes the gene Deleted in Colorectal Cancer (DCC), has been linked to colorectal and many other human cancers. DCC encodes the receptor for the axon guidance molecule Netrin (Net) and functions during neural development in a variety of organisms. However, since its discovery in the 1990s, the status of DCC as a tumor suppressor has been debated, primarily due to a lack of support for this hypothesis in animal models. A recent study from our laboratory capitalized on the genetic tractability of Drosophila melanogaster to demonstrate that this gene functions as an invasive tumor suppressor, thereby providing the first direct link between DCC loss and metastatic phenotypes in an animal model for cancer. Two subsequent studies from other laboratories have demonstrated that DCC suppresses tumor progression and metastasis in murine colorectal and mammary tumor models. Combined, these findings have prompted the rebirth of DCC as a tumor suppressor and highlighted the need for continued analysis of DCC function in animal models for human cancer.

Original languageEnglish
Pages (from-to)1445-1453
Number of pages9
JournalCurrent Drug Targets
Volume13
Issue number11
DOIs
StatePublished - 2012

Fingerprint

Tumors
Colorectal Neoplasms
Genes
Animals
Neoplasms
Animal Models
Chromosomes
Axon Guidance
Axons
Loss of Heterozygosity
Human Chromosomes
Drosophila melanogaster
Molecules
Breast Neoplasms
Neoplasm Metastasis
Phenotype

Keywords

  • Apoptosis
  • Axon guidance
  • Cancer
  • DCC
  • Drosophila melanogaster
  • Metastasis
  • Netrin
  • Tumor suppressor

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology
  • Clinical Biochemistry
  • Molecular Medicine

Cite this

Deleted in Colorectal Cancer (DCC) pathfinding : Axon guidance gene finally turned tumor suppressor. / Scheel, Molly.

In: Current Drug Targets, Vol. 13, No. 11, 2012, p. 1445-1453.

Research output: Contribution to journalArticle

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