Integration of microenvironmental and stress signaling antagonizes colorectal cancer progression

EMBO J. 2014 Aug 18;33(16):1737-9. doi: 10.15252/embj.201489364. Epub 2014 Jul 14.

Abstract

Genetic alterations can drive oncogenic events and cancer development. However, this is only half of the story. It is now evident that tumor progression only occurs if powerful stress signaling pathways and microenvironmental signals are overcome. Two recent Nature Cell Biology papers study how niche signals of primary and target organ barriers have to be overridden for oncogenes to allow for colorectal cancer (CRC) initiation and metastasis (Urosevic et al, 2014; Whissell et al, 2014).

Publication types

  • Comment

MeSH terms

  • Adenoma*
  • Animals
  • Bone Morphogenetic Protein Receptors / genetics*
  • Colonic Neoplasms / pathology*
  • Colorectal Neoplasms / physiopathology*
  • Female
  • GATA6 Transcription Factor / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Liver Neoplasms / secondary*
  • Lung Neoplasms / secondary*
  • Male
  • Neoplasm Metastasis*
  • Parathyroid Hormone-Related Protein / metabolism*
  • Signal Transduction*
  • Stem Cells / cytology*
  • Stem Cells / metabolism*
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • GATA6 Transcription Factor
  • Parathyroid Hormone-Related Protein
  • p38 Mitogen-Activated Protein Kinases
  • Bone Morphogenetic Protein Receptors