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Verteporfin inhibits gastric cancer cell growth by suppressing adhesion molecule FAT1

Myoung-Hee Kang1,2, Gi Seok Jeong3, Duane T Smoot4

  • 1Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea.

Oncotarget
|December 13, 2017
PubMed

Insights

Verteporfin (VP) effectively inhibits gastric cancer (GC) cell growth by targeting FAT1, a molecule promoting cell invasion and metastasis. This suggests VP is a promising therapeutic strategy for treating advanced gastric cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Repurposing

Background:

  • Gastric cancer (GC) remains a significant global health challenge, necessitating novel targeted therapies.
  • Existing treatments for GC have limitations, driving the search for innovative therapeutic strategies.

Purpose of the Study:

  • To investigate the anti-cancer effects of verteporfin (VP), a repurposed drug, on gastric cancer cell lines.
  • To elucidate the molecular mechanisms underlying VP's action in GC, focusing on gene expression changes.

Main Methods:

  • Utilized various GC cell lines for drug sensitivity testing.
  • Performed gene expression profiling to identify genes affected by VP treatment.
  • Conducted gene silencing experiments to validate the role of FAT1.

Main Results:

  • Verteporfin (VP) demonstrated significant inhibition of proliferation across multiple GC cell lines.
  • VP treatment led to down-regulation of genes associated with cell migration and oncogenic functions, notably FAT1.
  • Silencing FAT1 mimicked VP's effects, reducing cell migration and invasion.
  • Elevated FAT1 expression correlated with poorer prognosis in GC patients.

Conclusions:

  • Verteporfin (VP) exhibits potent anti-gastric cancer activity by suppressing cell migration and invasion.
  • Targeting FAT1 with VP represents a promising therapeutic avenue for inhibiting GC metastasis.
Keywords:
FAT1gastric cancermetastasisverteporfin

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