Reactive oxygen species up-regulate p53 and Puma; a possible mechanism for apoptosis during combined treatment with TRAIL and wogonin

Br J Pharmacol. 2009 Aug;157(7):1189-202. doi: 10.1111/j.1476-5381.2009.00245.x. Epub 2009 May 11.

Abstract

Background and purpose: Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) triggers apoptotic death in a variety of cancer cells without marked toxicity to most normal cells. We previously reported that wogonin, a potent anticancer agent from a Chinese herb, up-regulates p53 in prostate cancer cells. In this study, the effects of combinations of TRAIL and wogonin on a human prostate cancer cell line LNCaP, resistant to TRAIL, was evaluated for evidence of synergy in triggering apoptosis.

Experimental approach: Western blot assay and the 'comet' assay were used to study the underlying mechanisms of cell death and search for any mechanisms of enhancement of TRAIL-induced apoptosis in the presence of wogonin.

Key results: During combined treatment with wogonin and TRAIL, cytotoxicity, poly(ADP-ribose) polymerase cleavage and caspase activation were associated with up-regulation of p53 through DNA damage and reactive oxygen species (ROS) generation. N-acetylcysteine (NAC), an antioxidant, inhibited ROS generation and synergistic interaction between TRAIL and wogonin. Experimental results in human colon cancer HCT116 cells demonstrated that p53-dependent Puma up-regulation played an important role; deficiency in either p53 or Puma prevented wogonin-enhanced TRAIL-induced apoptosis.

Conclusions and implications: The present studies suggest that wogonin enhances TRAIL-induced cytotoxicity through up-regulation of p53 and Puma, mediated by ROS.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Antioxidants / pharmacology*
  • Apoptosis / physiology*
  • Apoptosis Regulatory Proteins / biosynthesis*
  • Apoptosis Regulatory Proteins / genetics
  • Caspases / metabolism
  • Cell Line, Tumor
  • DNA Damage
  • Drug Synergism
  • Enzyme Activation
  • Flavanones / pharmacology*
  • Gene Knockdown Techniques
  • Histones / metabolism
  • Humans
  • Male
  • Phosphorylation
  • Prostatic Neoplasms
  • Proto-Oncogene Proteins / biosynthesis*
  • Proto-Oncogene Proteins / genetics
  • RNA, Small Interfering / genetics
  • Reactive Oxygen Species / metabolism*
  • Recombinant Proteins / pharmacology
  • TNF-Related Apoptosis-Inducing Ligand / pharmacology*
  • Tumor Suppressor Protein p53 / biosynthesis*
  • Tumor Suppressor Protein p53 / genetics
  • Up-Regulation
  • bcl-2-Associated X Protein / physiology

Substances

  • Antineoplastic Agents
  • Antioxidants
  • Apoptosis Regulatory Proteins
  • BAX protein, human
  • BBC3 protein, human
  • Flavanones
  • H2AX protein, human
  • Histones
  • Proto-Oncogene Proteins
  • RNA, Small Interfering
  • Reactive Oxygen Species
  • Recombinant Proteins
  • TNF-Related Apoptosis-Inducing Ligand
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein
  • Caspases
  • wogonin