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Interaction between N-cadherin and decoy receptor-2 regulates apoptosis in head and neck cancer

Phuong Thao Nguyen1,2,3, Dung Nguyen1, Chanbora Chea1

  • 1Department of Oral and Maxillofacial Pathobiology, Basic Life Science, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Oncotarget
|August 25, 2018
PubMed

Insights

N-cadherin promotes head and neck cancer growth by blocking apoptosis. It increases decoy receptor DcR-2 and decreases death receptor DR-5, aiding tumor cell survival and chemotherapy resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • N-cadherin, a neural cell adhesion molecule, is implicated in head and neck squamous cell carcinoma (HNSCC) progression.
  • Tumor cells evade apoptosis, a key mechanism for cancer cell survival and growth.
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors, including death receptors (DR-4, DR-5) and decoy receptors (DcR-1, DcR-2), regulate apoptosis.

Purpose of the Study:

  • To elucidate the mechanism by which N-cadherin promotes cancer cell growth in HNSCC.
  • To investigate the role of N-cadherin in regulating TRAIL receptor expression and apoptosis.
  • To determine the functional interaction between N-cadherin and TRAIL receptors in HNSCC survival.

Main Methods:

  • Analysis of N-cadherin, DR-5, and DcR-2 expression in HNSCC cells and patient specimens.
  • N-cadherin knockdown and overexpression experiments.
  • Assessment of apoptotic index and cell signaling pathways (MAPK/ERK, NF-kB).
  • Co-immunoprecipitation to confirm N-cadherin and DcR-2 interaction.

Main Results:

  • N-cadherin overexpression upregulated DcR-2 and downregulated DR-5, while N-cadherin knockdown had the opposite effect.
  • A positive correlation was observed between N-cadherin and DcR-2 expression in HNSCC specimens with low apoptotic indices.
  • N-cadherin directly interacts with DcR-2, leading to suppressed apoptosis via MAPK/ERK activation and inhibited NF-kB signaling.
  • This interaction contributes to chemotherapy resistance by protecting cancer cells from apoptosis.

Conclusions:

  • N-cadherin enhances HNSCC growth by inhibiting apoptosis through modulation of TRAIL receptor expression.
  • The interaction between N-cadherin and DcR-2 plays a critical role in promoting cancer cell survival and chemoresistance.
  • Targeting N-cadherin or its interaction with DcR-2 may represent a therapeutic strategy for HNSCC.
Keywords:
DR-5, DcR-2N-cadherinanti-apoptosisdeath receptors

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