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Soluble E-cadherin: a critical oncogene modulating receptor tyrosine kinases, MAPK and PI3K/Akt/mTOR signaling

S M Brouxhon1, S Kyrkanides1, X Teng1

  • 1Department of Emergency Medicine, Health Sciences Center, Stony Brook University, Stony Brook, NY, USA.

Oncogene
|January 16, 2013
PubMed

Insights

Soluble E-cadherin (sEcad) fragments promote skin cancer growth and spread by activating growth factor receptor pathways. Inhibiting these pathways suppressed sEcad

Area of Science:

  • Oncology
  • Molecular Biology
  • Dermatology

Background:

  • E-cadherin, a cell adhesion glycoprotein, is often lost during cancer progression.
  • A soluble fragment, sEcad, is found at higher levels in cancer patients' bodily fluids.
  • The role of sEcad in skin squamous cell carcinoma (SCC) progression was previously unclear.

Purpose of the Study:

  • To investigate the functional role of soluble E-cadherin (sEcad) in skin squamous cell carcinoma (SCC) progression.
  • To explore the molecular mechanisms by which sEcad influences tumor growth and metastasis.
  • To identify sEcad as a potential therapeutic target for cutaneous SCCs.

Main Methods:

  • Analysis of E-cadherin and sEcad levels in human SCC samples and UV-induced mouse SCC models.
  • Investigated the association of sEcad with human epidermal growth factor receptor (HER) and insulin-like growth factor-1 receptor (IGF-1R) families.
  • Assessed the impact of sEcad on mitogen-activated protein kinase (MAPK) and PI3K/Akt/mTOR signaling pathways in vitro.
  • Evaluated the effects of sEcad on tumor growth, motility, and invasion, including matrix metalloproteinase-2 (MMP-2) and MMP-9 activation.
  • Tested the efficacy of HER, PI3K, or MEK inhibitors in blocking sEcad-mediated tumorigenic effects.

Main Results:

  • Decreased full-length E-cadherin and increased sEcad were observed in human SCCs and mouse models.
  • sEcad was found to associate with HER and IGF-1R family members in tumors.
  • sEcad activated MAPK and PI3K/Akt/mTOR signaling pathways, enhancing proliferation, migration, and invasion via MMP-2/MMP-9.
  • Inhibitors targeting HER, PI3K, or MEK effectively suppressed sEcad's pro-tumorigenic activities.

Conclusions:

  • Soluble E-cadherin (sEcad) significantly contributes to skin carcinogenesis.
  • sEcad promotes SCC progression by interacting with HER/IGF-1R receptors and activating MAPK and PI3K/Akt/mTOR pathways.
  • sEcad represents a promising therapeutic target for treating cutaneous squamous cell carcinomas.

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