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Regulation of Soluble E-Cadherin Signaling in Non-Small-Cell Lung Cancer Cells by Nicotine, BDNF, and β-Adrenergic

Ravel Ray1, Stuti Goel1, Hind Al Khashali1

  • 1Chemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.

Biomedicines
|September 28, 2023
PubMed

Insights

Soluble E-cadherin (sE-cad) levels increase with certain lung cancer cell treatments, mediated by MMP9. sE-cad affects cell signaling and viability in A549 cells but not H1299 cells.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Cancer Research

Background:

  • E-cadherin is crucial for cell adhesion, and its soluble form (sE-cad) may impact cancer progression.
  • Matrix metalloproteinases (MMPs), particularly MMP9, are implicated in E-cadherin cleavage.
  • Previous work showed BDNF and nicotine increase non-small cell lung cancer (NSCLC) cell viability.

Purpose of the Study:

  • To investigate the role of MMP9 and sE-cad in NSCLC cell lines (A549 and H1299).
  • To determine the effect of specific treatments (BDNF, nicotine, epinephrine, propranolol) on MMP9 and sE-cad levels.
  • To elucidate the functional impact of sE-cad on cell signaling and viability.

Main Methods:

  • Treatment of A549 and H1299 NSCLC cell lines with BDNF, nicotine, epinephrine, and propranolol.
  • Measurement of MMP9 and sE-cad levels in cell media.
  • MMP9 knockdown experiments in A549 cells.
  • Immunodepletion of sE-cad and assessment of downstream signaling pathways (EGFR, IGF-1R, PI3K, ERK1/2, p53) and cell viability/apoptosis.

Main Results:

  • BDNF, nicotine, or epinephrine increased MMP9 and sE-cad levels in A549 and H1299 cells, an effect reversed by propranolol.
  • MMP9 levels positively correlated with sE-cad levels in A549 cells.
  • sE-cad depletion in A549 cells reduced EGFR/IGF-1R activation, decreased PI3K/ERK1/2 activity, increased p53 activation, and reduced cell viability while increasing apoptosis.
  • These functional effects of sE-cad were not observed in H1299 cells.

Conclusions:

  • MMP9 mediates the release of sE-cad in response to specific stimuli in NSCLC cells.
  • sE-cad plays a functional role in regulating cell signaling pathways and viability in A549 cells, but not H1299 cells.
  • These findings highlight cell-specific roles of sE-cad in NSCLC and suggest potential therapeutic targets.
Keywords:
BDNFEGFRERK1/2IGF-1RPI3Klung cancermatrix metalloproteasesnicotinenicotinic acetylcholine receptorsp53soluble E-cadherinβ-adrenergic receptors

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