Leptin stimulates esophageal adenocarcinoma growth by nonapoptotic mechanisms

Am J Surg. 2003 Nov;186(5):575-8. doi: 10.1016/j.amjsurg.2003.07.017.


Background: Leptin is a hormone primarily produced by adipocytes and serum leptin is elevated in obese persons. One risk factor associated with adenocarcinoma of the esophagus is obesity. We hypothesized that leptin would have stimulatory effects on esophageal adenocarcinoma and alter apoptosis in vitro.

Methods: Barrett's esophageal adenocarcinoma cells (BIC-1 and SEG-1) were cultured with human recombinant leptin (80 ng/mL) for 24 hours. Cell growth was determined by MTT assay. Apoptosis and necrosis was measured after 16 hours of treatment with leptin using a Cell Death Kit.

Results: Exogenous leptin stimulated cell proliferation in both cell lines. No changes in apoptosis or necrosis resulted between control and leptin-treated groups.

Conclusions: We have shown that leptin increases the proliferation of human esophageal adenocarcinoma, but does not alter cell apoptosis or necrosis. The data suggest that leptin stimulates esophageal adenocarcinoma growth by nonapoptotic mechanisms. Leptin antagonism may have potential efficacy in esophageal cancer therapy.

MeSH terms

  • Adenocarcinoma / pathology*
  • Apoptosis
  • Barrett Esophagus / pathology*
  • Cell Division / drug effects
  • Enzyme-Linked Immunosorbent Assay
  • Esophageal Neoplasms / pathology*
  • Humans
  • Leptin / pharmacology*
  • Necrosis
  • Recombinant Proteins / pharmacology
  • Stimulation, Chemical
  • Tumor Cells, Cultured / drug effects


  • Leptin
  • Recombinant Proteins