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α-Mangostin suppresses human gastric adenocarcinoma cells in vitro via blockade of Stat3 signaling pathway.

Shan T, Cui XJ, Li W, Lin WR, Lu HW, Li YM, Chen X, Wu T - Acta Pharmacol. Sin. (2014)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710004, China.

ABSTRACT

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.

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Related in: MedlinePlus

(A) Effect of α-mangostin on cellular apoptosis. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL). After 6, 18, and 24 h, cellular apoptosis was examined for by Annexin V-PI double-labeling and FACS analysis. (B) TUNEL assay showing the apoptotic effect of α-mangostin on cells. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL) for 6, 18, and 24 h. The results are representative of three independent experiments. (C) Alpha-mangostin-induced typical chromatin offset and apoptotic body formation gradually in BGC-823 and SGC-7901 cells. Cells were incubated with α-mangostin (7 μg/mL) after 6, 18, and 24 h, and cellular morphologic changes were examined by transmission electron microscopy (×6000–10000). The results are representative of three independent experiments.
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fig2: (A) Effect of α-mangostin on cellular apoptosis. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL). After 6, 18, and 24 h, cellular apoptosis was examined for by Annexin V-PI double-labeling and FACS analysis. (B) TUNEL assay showing the apoptotic effect of α-mangostin on cells. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL) for 6, 18, and 24 h. The results are representative of three independent experiments. (C) Alpha-mangostin-induced typical chromatin offset and apoptotic body formation gradually in BGC-823 and SGC-7901 cells. Cells were incubated with α-mangostin (7 μg/mL) after 6, 18, and 24 h, and cellular morphologic changes were examined by transmission electron microscopy (×6000–10000). The results are representative of three independent experiments.

Mentions: To establish whether the anti-proliferation effect of α-mangostin is induced by apoptosis, we tested the apoptotic rate of two cell lines with a flow cytometry assay. BGC-823 and SGC-7901 cells were treated with α-mangostin (7 μg/mL) for 6, 18, and 24 h. Alpha-mangostin increased the apoptosis index in a time-dependent manner compared with control (P<0.05; Figure 2A).


α-Mangostin suppresses human gastric adenocarcinoma cells in vitro via blockade of Stat3 signaling pathway.

Shan T, Cui XJ, Li W, Lin WR, Lu HW, Li YM, Chen X, Wu T - Acta Pharmacol. Sin. (2014)

(A) Effect of α-mangostin on cellular apoptosis. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL). After 6, 18, and 24 h, cellular apoptosis was examined for by Annexin V-PI double-labeling and FACS analysis. (B) TUNEL assay showing the apoptotic effect of α-mangostin on cells. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL) for 6, 18, and 24 h. The results are representative of three independent experiments. (C) Alpha-mangostin-induced typical chromatin offset and apoptotic body formation gradually in BGC-823 and SGC-7901 cells. Cells were incubated with α-mangostin (7 μg/mL) after 6, 18, and 24 h, and cellular morphologic changes were examined by transmission electron microscopy (×6000–10000). The results are representative of three independent experiments.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4125713&req=5

fig2: (A) Effect of α-mangostin on cellular apoptosis. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL). After 6, 18, and 24 h, cellular apoptosis was examined for by Annexin V-PI double-labeling and FACS analysis. (B) TUNEL assay showing the apoptotic effect of α-mangostin on cells. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL) for 6, 18, and 24 h. The results are representative of three independent experiments. (C) Alpha-mangostin-induced typical chromatin offset and apoptotic body formation gradually in BGC-823 and SGC-7901 cells. Cells were incubated with α-mangostin (7 μg/mL) after 6, 18, and 24 h, and cellular morphologic changes were examined by transmission electron microscopy (×6000–10000). The results are representative of three independent experiments.
Mentions: To establish whether the anti-proliferation effect of α-mangostin is induced by apoptosis, we tested the apoptotic rate of two cell lines with a flow cytometry assay. BGC-823 and SGC-7901 cells were treated with α-mangostin (7 μg/mL) for 6, 18, and 24 h. Alpha-mangostin increased the apoptosis index in a time-dependent manner compared with control (P<0.05; Figure 2A).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710004, China.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus