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Induction of Apoptosis in Human Leukemic Cell Lines by Diallyl Disulfide via Modulation of EGFR/ERK/PKM2 Signaling Pathways

  • Luo, Nian (Laboratory of Stem Cells and Tissue Engineering, Histology and Embryology, Chongqing Medical University) ;
  • Zhao, Lv-Cui (Laboratory of Stem Cells and Tissue Engineering, Histology and Embryology, Chongqing Medical University) ;
  • Shi, Qing-Qiang (Laboratory of Stem Cells and Tissue Engineering, Histology and Embryology, Chongqing Medical University) ;
  • Feng, Zi-Qiang (Laboratory of Stem Cells and Tissue Engineering, Histology and Embryology, Chongqing Medical University) ;
  • Chen, Di-Long (Laboratory of Stem Cells and Tissue Engineering, Histology and Embryology, Chongqing Medical University) ;
  • Li, Jing (Laboratory of Stem Cells and Tissue Engineering, Histology and Embryology, Chongqing Medical University)
  • Published : 2015.04.29

Abstract

Background: Diallyl disulfide (DADS) may exert potent anticancer action both in vitro and in vivo. Although its effects on cancer are significant, the underlying mechanisms remain unknown. In this study, we sought to elucidate possible links between DADS and pyruvate kinase (PKM2). Materials and Methods: $KG1{\alpha}$, a leukemia cell line highly expressing PKM2 was used with a cell counting kit (CCK)-8 and flow cytometry (FCM) to investigate the effects of DADS. Relationships between PKM2 and DADS associated with phosphorylation of EGFR, ERK1/2 and MEK, were assessed by western blot analysis. Results: In $KG1{\alpha}$ cells highly expressing PKM2, we found that DADS could affect proliferation, apoptosis and EGFR/ERK/PKM2 signaling pathways, abrogating EGF-induced nuclear accumulation of PKM2. Conclusions: These results suggested that DADS suppressed the proliferation of $KG1{\alpha}$ cells, providing evidence that its proapoptotic effects are mediated through the inhibition of EGFR/ERK/PKM2 signaling pathways.

Keywords

Diallyl disulfide;leukemia cells;pyruvate kinase M2;apoptosis;EGFR/ERK/PKM2 signaling pathways

Acknowledgement

Supported by : National Natural Science Foundation of China

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