Maslinic acid induced apoptosis in bladder cancer cells through activating p38 MAPK signaling pathway

Mol Cell Biochem. 2014 Jul;392(1-2):281-7. doi: 10.1007/s11010-014-2038-y. Epub 2014 Apr 1.

Abstract

Bladder cancer is among the most aggressive human malignant carcinoma and always showed resistance to traditional chemotherapy based on DNA damaging drugs. Unlike the existing drugs that damage nuclear acid molecules, maslinic acid (MA) displays anti-tumor function in various types of cancers by targeting specific intracellular signaling pathways and is regarded as a promising agent for future clinical cancer therapy. However, its effect on bladder cancer is still unknown. In this study, we assessed the influence of MA on survival of bladder cancer cells and the involved mechanisms. MTT assay showed that MA suppressed the viability of bladder cancer cells. We further confirmed the growth-suppressing activity of MA on T24 and 253J xenograft tumor in mouse models. Subsequently, we found that MA induced apoptosis in bladder cancer cells. Based on immunoblotting assay, we determined that p38 MAPK pathway was greatly activated in MA-treated bladder cancer cells. SB203580 inhibition of p38 MAPK rescued the MA-induced apoptosis of bladder cancer cells. In conclusion, we provided evidences that MA efficiently suppressed activation of p38 MAPK pathways and induced apoptosis of bladder cancer cells.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Cell Line, Tumor
  • Humans
  • MAP Kinase Signaling System*
  • Mice
  • Mice, Nude
  • Triterpenes / pharmacology*
  • Urinary Bladder Neoplasms / enzymology
  • Urinary Bladder Neoplasms / pathology*
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • Triterpenes
  • maslinic acid
  • p38 Mitogen-Activated Protein Kinases