PMID- 27802587
OWN - NLM
STAT- MEDLINE
DCOM- 20170426
LR  - 20240204
IS  - 0219-1032 (Electronic)
IS  - 1016-8478 (Print)
IS  - 1016-8478 (Linking)
VI  - 39
IP  - 10
DP  - 2016 Oct
TI  - Equol Induces Mitochondria-Dependent Apoptosis in Human Gastric Cancer Cells via 
      the Sustained Activation of ERK1/2 Pathway.
PG  - 742-749
AB  - The cancer chemo-preventive effects of equol have been demonstrated for a wide 
      variety of experimental tumours. In a previous study, we found that equol 
      inhibited proliferation and induced apoptotic death of human gastric cancer 
      MGC-803 cells. However, the mechanisms underlying equol-mediated apoptosis have 
      not been well understood. In the present study, the dual AO (acridine orange)/EB 
      (ethidium bromide) fluorescent assay, the comet assay, MTS, western blotting and 
      flow cytometric assays were performed to further investigate the pro-apoptotic 
      effect of equol and its associated mechanisms in MGC-803 cells. The results 
      demonstrated that equol induced an apoptotic nuclear morphology revealed by AO/EB 
      staining, the presence of a comet tail, the cleavage of caspase-3 and PARP and 
      the depletion of cIAP1, indicating its pro-apoptotic effect. In addition, 
      equol-induced apoptosis involves the mitochondria-dependent cell-death pathway, 
      evidenced by the depolarization of the mitochondrial membrane potential, the 
      cleavage of caspase-9 and the depletion of Bcl-xL and full-length Bid. Moreover, 
      treating MGC-803 cells with equol induced the sustained activation of 
      extracellular signal-regulated kinase (ERK), and inhibiting ERK by U0126, a 
      MEK/ERK pathway inhibitor, significantly attenuated the equol-induced cell 
      apoptosis. These results suggest that equol induces mitochondria-dependent 
      apoptosis in human gastric cancer MGC-803 cells via the sustained activation of 
      the ERK1/2 pathway. Therefore, equol may be a novel candidate for the 
      chemoprevention and therapy of gastric cancer.
FAU - Yang, Zhiping
AU  - Yang Z
AD  - The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003 P.R. 
      China.
FAU - Zhao, Yan
AU  - Zhao Y
AD  - The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003 P.R. 
      China.
FAU - Yao, Yahong
AU  - Yao Y
AD  - The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003 P.R. 
      China.
FAU - Li, Jun
AU  - Li J
AD  - The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003 P.R. 
      China.
FAU - Wang, Wangshi
AU  - Wang W
AD  - The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003 P.R. 
      China.
FAU - Wu, Xiaonan
AU  - Wu X
AD  - Xiamen Medical College, Xiamen, Fujian 350108, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20161031
PL  - United States
TA  - Mol Cells
JT  - Molecules and cells
JID - 9610936
RN  - 0 (Phytoestrogens)
RN  - 531-95-3 (Equol)
SB  - IM
MH  - Apoptosis/drug effects
MH  - Cell Line, Tumor
MH  - Enzyme Activation
MH  - Equol/*pharmacology
MH  - Humans
MH  - MAP Kinase Signaling System/*drug effects
MH  - Mitochondria/*drug effects/metabolism
MH  - Phytoestrogens/*pharmacology
MH  - Stomach Neoplasms/enzymology/*genetics/pathology
PMC - PMC5104882
OTO - NOTNLM
OT  - ERK signalling pathway
OT  - equol
OT  - gastric cancer
OT  - mitochondria-dependent apoptosis
EDAT- 2016/11/03 06:00
MHDA- 2017/04/27 06:00
PMCR- 2016/10/31
CRDT- 2016/11/03 06:00
PHST- 2016/06/29 00:00 [received]
PHST- 2016/09/01 00:00 [revised]
PHST- 2016/09/22 00:00 [accepted]
PHST- 2016/11/03 06:00 [pubmed]
PHST- 2017/04/27 06:00 [medline]
PHST- 2016/11/03 06:00 [entrez]
PHST- 2016/10/31 00:00 [pmc-release]
AID - S1016-8478(23)05096-3 [pii]
AID - molce-39-10-742 [pii]
AID - 10.14348/molcells.2016.0162 [doi]
PST - ppublish
SO  - Mol Cells. 2016 Oct;39(10):742-749. doi: 10.14348/molcells.2016.0162. Epub 2016 
      Oct 31.