Induction of apoptotic cell death by 2'-hydroxycinnamaldehyde is involved with ERK-dependent inactivation of NF-kappaB in TNF-alpha-treated SW620 colon cancer cells

Biochem Pharmacol. 2005 Oct 15;70(8):1147-57. doi: 10.1016/j.bcp.2005.07.028.


2'-Hydroxycinnamaldehyde (HCA) inhibits cell growth of several human cancer cells with unknown mechanisms. We investigated the inhibitory effect of HCA on TNF-alpha-induced cell growth and possible signal pathway in SW620 colon cancer cells. HCA inhibited TNF-alpha-induced SW620 colon cell growth in time- and dose-dependent manner through induction of apoptotic cell death. Parallel with inhibitory effect on cell growth, HCA dose dependency inhibited TNF-alpha-induced activation of NF-kappaB accompanied with inhibition of the translocation of p50. HCA also induced expression of caspase-3 and Bax, but decreased Bcl-2. HCA furthermore activated ERK pathway, and ERK inhibitor reversed inhibitory effect of HCA on cell growth and transcriptional activation of NF-kappaB. These results demonstrate that HCA inhibits cell growth through induction of apoptotic cell death by ERK pathway-dependent NF-kappaB inactivation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Blotting, Western
  • Cell Line, Tumor
  • Cinnamates / pharmacology*
  • Colonic Neoplasms / enzymology
  • Colonic Neoplasms / pathology*
  • Electrophoretic Mobility Shift Assay
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Humans
  • NF-kappa B / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / pharmacology*


  • Cinnamates
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • p-hydroxycinnamaldehyde
  • Extracellular Signal-Regulated MAP Kinases