Anti-tumor activity of the X-linked inhibitor of apoptosis (XIAP) inhibitor embelin in gastric cancer cells

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• 作者：Da-Guang Wang (1)
  Ya-Bin Sun (2)
  Fei Ye (3)
  Wei Li (1)
  Punyaram Kharbuja (1)
  Ling Gao (4)
  David Y. Zhang (3)
  Jian Suo (1)
  
• 关键词：Embelin ; Gastric cancer ; Apoptosis ; XIAP ; Ingenuity pathway analysis
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2014
• 出版时间：January 2014
• 年：2014
• 卷：386
• 期：1-2
• 页码：143-152
• 全文大小：
• 作者单位：Da-Guang Wang (1)
  Ya-Bin Sun (2)
  Fei Ye (3)
  Wei Li (1)
  Punyaram Kharbuja (1)
  Ling Gao (4)
  David Y. Zhang (3)
  Jian Suo (1)
  
  1. Department of General Surgery, The First Hospital, Jilin University, Changchun, 130021, Jilin, China
  2. Department of Ophthalmology, The First Hospital, Jilin University, Changchun, 130021, Jilin, China
  3. Department of Pathology, Mount Sinai School of Medicine, New York, NY, 10029, USA
  4. Department of Cancer Center, The First Hospital, Jilin University, Changchun, 130021, Jilin, China
  
• ISSN：1573-4919

文摘

This study investigated the anticancer effects of embelin in human gastric cancer cells and the underlying molecular mechanisms. Gastric cancer cells were treated with embelin and 5-FU for methyl-thiazolyl-tetrazolium bromide cell viability assay and flow cytometric detection of cell viability and apoptosis. Protein pathway array (PPA) and Western blot were used to investigate differentially expressed proteins in embelin-treated gastric cancer cells. Embelin reduced gastric cancer cell viability, induced apoptosis, and enhanced 5-FU antitumor activity in gastric cancer cells. Mechanistically, embelin induced cell cycle arrest at the S and G2/M phases. Molecularly, embelin downregulated expression of X-linked inhibitor of apoptosis and cell cycle-regulatory proteins, such as CDK1, CDC25B, CDC25C, cyclinB1, and CDK2. PPA analysis showed that embelin modulated several pathways that are associated with cell growth and apoptosis, such as PI3K/AKT, JAK/STAT, p38 MAPK, and p53. The data from the current study implied that reduction of gastric cancer cell viability after treatment with embelin was through cell cycle arrest at the S and G2/M phases and apoptosis.