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Deadly crosstalk: Notch signaling at the intersection of EMT and cancer stem cells

Ingrid Espinoza1, Lucio Miele

  • 1Cancer Institute, University of Mississippi Medical Center, Jackson, MS, United States; Department of Biochemistry, University of Mississippi Medical Center, Jackson, MS, United States.

Cancer Letters
|August 27, 2013
PubMed

Insights

Notch signaling deregulation promotes cancer progression and epithelial-to-mesenchymal transition (EMT). Inhibiting Notch signaling may reverse EMT, offering a promising cancer treatment strategy.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Oncology

Background:

  • Notch signaling is crucial for cell fate, stem cell renewal, and tissue differentiation.
  • Deregulation of Notch signaling is implicated in cancer development, cancer stem cells, angiogenesis, and EMT.
  • Epithelial-to-mesenchymal transition (EMT) is a key process in tumor aggressiveness and metastasis.

Purpose of the Study:

  • To review the role of deregulated Notch signaling in EMT and tumor aggressiveness.
  • To explore the potential of Notch inhibition as a cancer therapy.
  • To highlight Notch signaling's impact on reversing or preventing EMT.

Main Methods:

  • Literature review of studies on Notch signaling, EMT, and cancer.
  • Analysis of evidence linking Notch pathway to cancer progression and metastasis.
  • Synthesis of findings on the therapeutic potential of Notch inhibitors.

Main Results:

  • Accumulated evidence links Notch signaling deregulation to EMT and increased tumor aggressiveness.
  • Notch pathway plays a significant role in promoting cancer stem cell properties and angiogenesis.
  • Interference with Notch signaling can potentially reverse or prevent EMT.

Conclusions:

  • Notch signaling deregulation is a critical factor in tumor progression and aggressiveness.
  • Targeting Notch signaling presents a viable therapeutic strategy for various cancers.
  • Notch inhibition may be effective in managing cancers by reversing EMT.
Keywords:
A Disintegrin And Metalloprotease 10/17ADAM10/17CBF-1, Suppressor of Hairless/LAG1CSCsCSLCancer stem cellsEGFREMTEndMTHedgehogHhN(EC)N(IC)N(TM)NF-κBNO SynthaseNotch extracellular domainNotch inhibitorsNotch intracellular domainNotch signalingNotch transmembrane domainOxide Nitric SynthasePDGF-DPlatelet-derived growth factor DTGF-βTie1-2Transforming growth factor betaTyrosine kinase with immunoglobulin-like and EGF-like domains 1-2VE-cadherinVEGFVascular Endothelial Growth FactorVascular endothelial cadherinZEB1Zinc finger E-box-binding homeobox 1cancer stem cellsendothelial mesenchymal transitionepidermal growth factor receptorepithelial mesenchymal transitionnuclear factor kappa-light-chain-enhancer of activated B cells

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