Epigenetic regulation of RTK signaling

Jennifer M Spangle1,2, Thomas M Roberts3,4,5

  • 1Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA.

Journal of Molecular Medicine (Berlin, Germany)
|June 8, 2017
PubMed

Insights

Epigenomic mechanisms, not just direct gene mutations, can hyperactivate receptor tyrosine kinase (RTK) signaling. These non-heritable changes contribute to cancer by altering cell growth and survival pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Receptor tyrosine kinase (RTK) signaling regulates cell proliferation, metabolism, and survival.
  • Hyperactivation of RTK pathways is common in cancers, often due to genomic alterations.
  • Non-heritable genomic modifications also contribute to aberrant RTK signaling.

Purpose of the Study:

  • To review epigenomic mechanisms driving RTK pathway hyperactivation in cancer.
  • To explore how these mechanisms contribute to cancer development and progression.

Main Methods:

  • Literature review focusing on epigenomic modifications.
  • Analysis of RTK signaling pathways and their dysregulation in cancer.
  • Integration of knowledge on non-heritable genomic changes and cancer biology.

Main Results:

  • Epigenomic alterations can lead to sustained RTK signaling independent of ligand binding.
  • These epigenetic changes affect key downstream effectors like Ras, PI3K/AKT, and Raf.
  • Non-heritable modifications provide an alternative route to oncogenic signaling.

Conclusions:

  • Epigenomic mechanisms play a significant role in RTK pathway hyperactivation in cancer.
  • Understanding these epigenetic contributions is crucial for developing novel cancer therapies.
  • Targeting epigenomic alterations may offer new strategies to combat RTK-driven cancers.

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