Celastrol inhibits gastric cancer growth by induction of apoptosis and autophagy

BMB Rep. 2014 Dec;47(12):697-702. doi: 10.5483/bmbrep.2014.47.12.069.

Abstract

Recently, the interest in natural products for the treatment of cancer is increasing because they are the pre-screened candidates. In the present study, we demonstrate the therapeutic effect of celastrol, a triterpene extracted from the root bark of Chinese medicine on gastric cancer. The proliferation of AGS and YCC-2 cells were most sensitively decreased in six kinds of gastric cancer cell lines after the treatment with celastrol. Celastrol inhibited the cell migration and increased G1 arrest in cell-cycle populations in both cell lines. The treatment with celastrol significantly induced autophagy and apoptosis and increased the expression of autophagy and apoptosis-related proteins. We also found an increase in phosphorylated AMPK following a decrease in all phosphorylated forms of AKT, mTOR and S6K after the treatment with celastrol. Moreover, gastric tumor burdens were reduced in a dose-dependent manner by celastrol administration in a xenografted mice model. Taken together, celastrol distinctly inhibits the gastric cancer cell proliferation and induces autophagy and apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Animals
  • Apoptosis / drug effects*
  • Apoptosis Regulatory Proteins / metabolism
  • Autophagy / drug effects*
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects*
  • G1 Phase Cell Cycle Checkpoints / drug effects
  • Humans
  • Mice
  • Mice, Nude
  • Pentacyclic Triterpenes
  • Phosphorylation / drug effects
  • Proto-Oncogene Proteins c-akt / metabolism
  • Ribosomal Protein S6 Kinases / metabolism
  • Signal Transduction / drug effects
  • Stomach Neoplasms / drug therapy
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology
  • TOR Serine-Threonine Kinases / metabolism
  • Transplantation, Heterologous
  • Triterpenes / therapeutic use
  • Triterpenes / toxicity*

Substances

  • Apoptosis Regulatory Proteins
  • Pentacyclic Triterpenes
  • Triterpenes
  • Proto-Oncogene Proteins c-akt
  • Ribosomal Protein S6 Kinases
  • TOR Serine-Threonine Kinases
  • AMP-Activated Protein Kinases
  • celastrol