Evodiamine, a novel inhibitor of the Wnt pathway, inhibits the self-renewal of gastric cancer stem cells

Int J Mol Med. 2015 Dec;36(6):1657-63. doi: 10.3892/ijmm.2015.2383. Epub 2015 Oct 21.

Abstract

Gastric cancer stem cells (GCSCs) have an important role in metastasis and recurrence of gastric cancer, and novel treatment strategies that target GCSCs are urgently required. Although evodiamine (Evo), a derivative of the traditional herbal medicine Evodia rutaecarpa, has been reported to have various biological effects, its effect on GCSCs remains unknown. In order to determine the effect of Evo on apoptosis of GCSCs, an MTS assay, flow cytometry and western blot analysis were performed. The effect of Evo on self‑renewal in GCSCs was measured by alterations in the sphere formation ability, the expression of induced‑pluripotent stem cell factors, expression of epithelial-to-mesenchymal transition (EMT) factors and oxaliplatin resistance of gastric cancer cells (GCCs). Evo inhibited proliferation, promoted the Bax/B‑cell lymphoma 2 ratio and altered active caspase‑3 expression of GCSCs. In addition, Evo decreased the sphere formation ability, the expression of Sox2, KLF4, Bmi‑1 and Oct4, and oxaliplatin resistance in GCCs. Evo decreased the expression of Slug, Twist, Zeb1 and vimentin, suggesting an inhibitory effect on EMT. Furthermore, the expression of β‑catenin, c‑Myc and cyclin D1 was decreased in Evo‑treated spheroids from GCCs. In conclusion, Evo inhibited the Wnt/β‑catenin signaling pathway to inhibit proliferation and stem cell properties of GCSCs and repressed the EMT. The present findings highlight the prospect of Evo as a CSCs-targeted therapy in gastric cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Cell Survival / drug effects
  • Cyclin D1 / metabolism
  • Epithelial-Mesenchymal Transition / drug effects
  • Flow Cytometry
  • Humans
  • Kruppel-Like Factor 4
  • Molecular Structure
  • Neoplastic Stem Cells / drug effects*
  • Neoplastic Stem Cells / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-myc / metabolism
  • Quinazolines / chemistry
  • Quinazolines / pharmacology*
  • Snail Family Transcription Factors
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology
  • Transcription Factors / metabolism
  • Twist-Related Protein 1 / metabolism
  • Wnt Signaling Pathway / drug effects*
  • bcl-2-Associated X Protein / metabolism
  • beta Catenin / metabolism

Substances

  • BAX protein, human
  • KLF4 protein, human
  • Kruppel-Like Factor 4
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-myc
  • Quinazolines
  • SNAI1 protein, human
  • Snail Family Transcription Factors
  • Transcription Factors
  • Twist-Related Protein 1
  • bcl-2-Associated X Protein
  • beta Catenin
  • Cyclin D1
  • evodiamine