Triptolide induces mitochondria-mediated apoptosis of Burkitt's lymphoma cell via deacetylation of GSK-3β by increased SIRT3 expression

Toxicol Appl Pharmacol. 2018 Mar 1:342:1-13. doi: 10.1016/j.taap.2018.01.011. Epub 2018 Feb 4.

Abstract

Burkitt's lymphoma (BL) is a highly aggressive B-cell non-Hodgkin lymphoma with rapid growth and dissemination propensity. Triptolide (TP), an active component extracted from Chinese herb Tripterygium wilfordii Hook f., has broad-spectrum anti-tumor activities. This study aimed to explore the in vitro and in vivo anti-cancer effects of TP on BL and the potential molecular mechanisms. In this study, the in vitro anti-tumor activity of TP was determined by CCK-8 and flow cytometry assays in Raji, NAMALWA and Daudi cells. The expression of SIRT3, phosphorylation and acetylation of glycogen synthase kinase-3β (GSK-3β) were analyzed by Western blot assay. Moreover, we examined the mitochondrial membrane potential by JC-1 method and measured apoptosis related protein using Western blot assay. BL xenograft model in NOD/SCID mice were established to evaluate the in vivo anti-cancer effect of TP. We discovered that TP inhibited BL cell growth and induced apoptosis in a dose-dependent manner. Loss of SIRT3 provides growth advances for BL cells. However, TP could up-regulate SIRT3 expression, which resulted in suppression of BL cells proliferation. GSK-3β was activated by SIRT3-mediated deacetylation, which subsequently induced mitochondrial translocation and accumulation of Bax and decrease of mitochondrial membrane potential. Anti-tumor studies in vivo showed that TP (0.36 mg/kg) inhibited the growth of BL xenografts in NOD/SCID mice with an inhibitory rate of 73.13%. Our data revealed that TP triggered mitochondrial apoptotic pathway in BL by increasing SIRT3 expression and activating SIRT3/GSK-3β/Bax pathway. This study indicated that TP is a potential anti-cancer Chinese herbal medicine against BL.

Keywords: Burkitt's lymphoma; GSK-3β; SIRT3; Triptolide; apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Apoptosis / drug effects
  • Burkitt Lymphoma / drug therapy
  • Burkitt Lymphoma / metabolism*
  • Burkitt Lymphoma / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Diterpenes / pharmacology*
  • Diterpenes / therapeutic use
  • Epoxy Compounds / pharmacology
  • Epoxy Compounds / therapeutic use
  • Glycogen Synthase Kinase 3 beta / metabolism*
  • Humans
  • Male
  • Membrane Potential, Mitochondrial / drug effects
  • Mice, Inbred NOD
  • Mice, SCID
  • Mitochondria / drug effects
  • Mitochondria / physiology
  • Phenanthrenes / pharmacology*
  • Phenanthrenes / therapeutic use
  • Sirtuin 3 / metabolism*
  • Tumor Burden / drug effects
  • bcl-2-Associated X Protein / metabolism

Substances

  • Antineoplastic Agents
  • Diterpenes
  • Epoxy Compounds
  • Phenanthrenes
  • bcl-2-Associated X Protein
  • triptolide
  • Glycogen Synthase Kinase 3 beta
  • SIRT3 protein, human
  • Sirtuin 3