TY - JOUR
T1 - Anti-tumor activity of the X-linked inhibitor of apoptosis (XIAP) inhibitor embelin in gastric cancer cells
AU - Wang, Da Guang
AU - Sun, Ya Bin
AU - Ye, Fei
AU - Li, Wei
AU - Kharbuja, Punyaram
AU - Gao, Ling
AU - Zhang, David Y.
AU - Suo, Jian
N1 - Funding Information:
Acknowledgments The authors wish to thank Dr. Goutham Narla of the Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine (New York, NY, USA), for gastric cancer cell line NCI-N87 (gastric carcinoma) and Mr. Yang Li for his excellent technical training in protein preparation. The study was supported in part by funding from The First Hospital, Jilin University, Changchun, China.
PY - 2014/1
Y1 - 2014/1
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Embelin
KW - Gastric cancer
KW - Ingenuity pathway analysis
KW - XIAP
UR - http://www.scopus.com/inward/record.url?scp=84891507798&partnerID=8YFLogxK
U2 - 10.1007/s11010-013-1853-x
DO - 10.1007/s11010-013-1853-x
M3 - Article
C2 - 24136460
AN - SCOPUS:84891507798
SN - 0300-8177
VL - 386
SP - 143
EP - 152
JO - Molecular and Cellular Biochemistry
JF - Molecular and Cellular Biochemistry
IS - 1-2
ER -