The inhibition of Wnt/β-catenin signaling pathway in human colon cancer cells by sulindac

Tumori. 2014 Jan-Feb;100(1):97-101. doi: 10.1700/1430.15823.

Abstract

The aberrant activation of Wnt/β-catenin signaling plays important roles in the initial development of colon cancer. Sulindac is a commonly used non-steroidal anti-inflammatory drug. We demonstrated the effects of sulindac on growth inhibition, apoptosis induction, and Wnt/β-catenin signaling suppression in human colon cancer cells. Sulindac significantly inhibited proliferation of HT-29 colon cancer cells in a dose- and time-dependent manner. Sulindac was found to induce the apoptosis of HT-29 cells and inhibit the Wnt/β-catenin pathway. The inhibition was further confirmed by the decreased protein levels of β-catenin. The results indicate that sulindac may play a beneficial role in the comprehensive treatment of colon cancer.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects
  • Blotting, Western
  • Caspase 3
  • Cell Proliferation / drug effects
  • Colorectal Neoplasms / drug therapy*
  • Colorectal Neoplasms / metabolism*
  • Colorectal Neoplasms / pathology
  • Colorimetry
  • Dose-Response Relationship, Drug
  • Flow Cytometry
  • HT29 Cells
  • Humans
  • Signal Transduction / drug effects*
  • Sulindac / pharmacology*
  • Time Factors
  • Wnt Proteins / drug effects
  • Wnt Proteins / metabolism*
  • beta Catenin / drug effects
  • beta Catenin / metabolism*

Substances

  • Antineoplastic Agents
  • CTNNB1 protein, human
  • Wnt Proteins
  • beta Catenin
  • Sulindac
  • Caspase 3