α-Mangostin suppresses human gastric adenocarcinoma cellsin vitro via blockade of Stat3 signaling pathway
Abstract
Tao SHAN1, *, Xi-juan CUI2, Wei LI3, Wan-run LIN4, Hong-wei LU1, Yi-ming LI1, Xi CHEN1, Tao WU1
1Department of General Surgery, Second Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an 710004, China; 2Department of General Surgery, First Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an 710061, China; 3Graduate School, Fourth Military Medical University, Xi’an 710033, China; 4Department of Pathology, Shandong Provincial Hospital, Ji’nan 250021, China
Aim: To investigate the anti-tumor effects of α-mangostin, a major xanthone identified in the pericarp of mangosteen (Garcinia mangostana Linn), against human gastric adenocarcinoma cells in vitro, and the mechanisms of the effects.
Methods: Human gastric adenocarcinoma cell lines BGC-823 and SGC-7901 were treated with α-mangostin. The cell viability was measured with MTT assay, and cell apoptosis was examined using flow cytometry and TUNEL assay. The expression of the relevant proteins was detected using Western blot.
Results: Treatment with α-mangostin (3–10 μg/mL) inhibited the viability of both BGC-823 and SGC-7901 cells in dose- and time-manners. Furthermore, α-mangostin (7 μg/mL) time-dependently increased the apoptosis index of the cancer cells, reduced the mitochondrial membrane potential of the cancer cells, and significantly increased the release of cytochrome c and AIF into cytoplasm. Moreover, the α-mangostin treatment markedly suppressed the constitutive Stat3 protein activation, and Stat3-regulated Bcl-xL and Mcl-1 protein levels in the cancer cells.
Conclusion: The anti-tumor effects of α-mangostin against human gastric adenocarcinoma cells in vitro can be partly attributed to blockade of Stat3 signaling pathway.
Keywords: gastric adenocarcinoma; anti-cancer drug; mangosteen; α-mangostin; apoptosis; mitochondria; Stat3; Bcl-xL; Mcl-1
The authors thank the staff of the Institution of Genetic Disease Research at Xi’an Jiaotong University for their technical assistance.
* To whom correspondence should be addressed.
E-mail shantao820304@163.com
Received 2014-02-04 Accepted 2014-05-12
Keywords:
1Department of General Surgery, Second Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an 710004, China; 2Department of General Surgery, First Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an 710061, China; 3Graduate School, Fourth Military Medical University, Xi’an 710033, China; 4Department of Pathology, Shandong Provincial Hospital, Ji’nan 250021, China
Aim: To investigate the anti-tumor effects of α-mangostin, a major xanthone identified in the pericarp of mangosteen (Garcinia mangostana Linn), against human gastric adenocarcinoma cells in vitro, and the mechanisms of the effects.
Methods: Human gastric adenocarcinoma cell lines BGC-823 and SGC-7901 were treated with α-mangostin. The cell viability was measured with MTT assay, and cell apoptosis was examined using flow cytometry and TUNEL assay. The expression of the relevant proteins was detected using Western blot.
Results: Treatment with α-mangostin (3–10 μg/mL) inhibited the viability of both BGC-823 and SGC-7901 cells in dose- and time-manners. Furthermore, α-mangostin (7 μg/mL) time-dependently increased the apoptosis index of the cancer cells, reduced the mitochondrial membrane potential of the cancer cells, and significantly increased the release of cytochrome c and AIF into cytoplasm. Moreover, the α-mangostin treatment markedly suppressed the constitutive Stat3 protein activation, and Stat3-regulated Bcl-xL and Mcl-1 protein levels in the cancer cells.
Conclusion: The anti-tumor effects of α-mangostin against human gastric adenocarcinoma cells in vitro can be partly attributed to blockade of Stat3 signaling pathway.
Keywords: gastric adenocarcinoma; anti-cancer drug; mangosteen; α-mangostin; apoptosis; mitochondria; Stat3; Bcl-xL; Mcl-1
The authors thank the staff of the Institution of Genetic Disease Research at Xi’an Jiaotong University for their technical assistance.
* To whom correspondence should be addressed.
E-mail shantao820304@163.com
Received 2014-02-04 Accepted 2014-05-12