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Growth Inhibition and Apoptosis Induction of Human Umbilical Vein Endothelial Cells by Apogossypolone

  • Zhan, Yong-Hua (School of Life Sciences and Technology, Xidian University) ;
  • Huang, Xiao-Feng (Central Laboratory, School of Basic Medicine, Fourth Military Medical University) ;
  • Hu, Xing-Bin (Department of Blood Transfusion, Xijing Hospital, Fourth Military Medical University) ;
  • An, Qun-Xing (Department of Blood Transfusion, Xijing Hospital, Fourth Military Medical University) ;
  • Liu, Zhi-Xin (Department of Blood Transfusion, Xijing Hospital, Fourth Military Medical University) ;
  • Zhang, Xian-Qing (Department of Blood Transfusion, Xijing Hospital, Fourth Military Medical University)
  • Published : 2013.03.30

Abstract

Aims and Background: Prostate cancer is one of the most common malignant tumors in the male reproductive system, which causes the second most cancer deaths of males, and control of angiogenesis in prostate lesions is of obvious importance. This study assessed the effect of apogossypolone (ApoG2) on proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs). Subjects and Methods: HUVECs were treated with different concentrations of ApoG2. The survival rate of HUVECs were determined by MTT assay. Utrastructural changes of HUVECs were assessed with transmission electron microscopy. Apoptosis in HUVECs was analyzed by flow cytometry and cell migration by Boyden chamber assay. Matrigel assays were used to quantify the development of tube-like networks. Results: ApoG2 significantly inhibited HUVEC growth even at 24 h (P<0.05). The inhibitory effect of ApoG2 is more obvious as the concentration and the culture time increased (P<0.05). These results indicate that ApoG2 inhibits the proliferation of HUVECs in a time- and concentration-dependent manner with increase of the apoptosis rate. Besides, ApoG2 reduced the formation of total pseudotubule length and network branches of HUVECs. Conclusions: The results suggest that ApoG2 inhibits angiogenesis of HUVECs by growth inhibition and apoptosis induction.

Keywords

References

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