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Updated: Aug 14, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Syntaphilin Regulates Epithelial-Mesenchymal Transition and Metastasis in Gastric Cancer via the FAK/NF-κB/MMP-9

Hye Jin Choi1, Jong Min Park1

  • 1College of Oriental Medicine, Daejeon University, Daejeon 34520, Republic of Korea.

International Journal of Molecular Sciences
|August 13, 2026
PubMed

Insights

Syntaphilin (SNPH) suppresses gastric cancer metastasis by inhibiting cell migration and invasion. Loss of SNPH promotes epithelial-mesenchymal transition (EMT) and invasion through the FAK/NF-κB/MMP-9 pathway.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Syntaphilin (SNPH) is increasingly recognized for its role in various cancers, beyond its initial classification as neuron-specific.
  • SNPH's known function involves inhibiting mitochondrial transport, which suppresses cancer cell migration and metastasis.
  • The precise mechanisms by which SNPH influences metastatic progression in different malignancies are not fully understood.

Purpose of the Study:

  • To investigate the role of Syntaphilin (SNPH) in the epithelial-mesenchymal transition (EMT) and invasiveness of gastric cancer cells.
  • To elucidate the molecular pathways modulated by SNPH in gastric cancer metastasis.

Main Methods:

  • Utilized SNPH knockdown and overexpression in SNU-638 gastric cancer cells.
  • Assessed cell migration and invasion capacities.
  • Analyzed the phosphorylation status of focal adhesion kinase (FAK) and nuclear factor kappa B (NF-κB).
  • Quantified the expression of EMT markers (vimentin) and transcription factors (Snail, Slug, Twist), and matrix metalloproteinase-9 (MMP-9) mRNA.

Main Results:

  • SNPH knockdown significantly enhanced gastric cancer cell migration (1.4-fold) and invasion (2.5-fold).
  • SNPH depletion led to increased FAK phosphorylation, vimentin upregulation, and elevated expression of Snail, Slug, and Twist.
  • SNPH deficiency induced NF-κB phosphorylation, subsequently upregulating MMP-9 mRNA expression and promoting extracellular matrix degradation.
  • Overexpression of SNPH reversed these pro-metastatic phenotypic and molecular changes.

Conclusions:

  • SNPH deficiency promotes gastric cancer cell migration and metastasis by driving EMT and invasion.
  • The FAK/NF-κB/MMP-9 signaling pathway is critically involved in SNPH-mediated regulation of gastric cancer invasion.
  • SNPH emerges as a potential novel biomarker and therapeutic target for reducing gastric cancer metastasis.
Keywords:
EMTFAKMMP-9gastric cancersyntaphilin

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