Smoothened inhibition leads to decreased proliferation and induces apoptosis in esophageal adenocarcinoma cells

Cancer Invest. 2013 Aug;31(7):480-9. doi: 10.3109/07357907.2013.820317.

Abstract

The Hedgehog (Hh) pathway is known to be active in Barrett's carcinogenesis. Therefore, we evaluated the efficacy and underlying mechanisms of inhibition of cancer cell growth by the smoothened (Smo) antagonist BMS-833923 in esophageal adenocarcinoma (EAC) cell lines. Cell proliferation and apoptosis were evaluated by flow cytometry, Western blotting, immunofluorescence, and quantitative reverse transcription polymerase chain reactions. Results showed that the Smo antagonist led to reduced Hh pathway activity, resulting in decreased cell proliferation and induction of apoptosis via the intrinsic pathway in the esophageal cancer cells. In conclusion, the Smo antagonist may have application as an EAC chemotherapeutic agent.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / metabolism*
  • Adenocarcinoma / pathology
  • Apoptosis / physiology*
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Proliferation
  • Esophageal Neoplasms / metabolism*
  • Esophageal Neoplasms / pathology
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Hedgehog Proteins / metabolism
  • Humans
  • Receptors, G-Protein-Coupled / antagonists & inhibitors*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / physiology
  • Smoothened Receptor

Substances

  • Hedgehog Proteins
  • Receptors, G-Protein-Coupled
  • SMO protein, human
  • Smoothened Receptor