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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

Anti-proliferative effect of α-mangostin (0 to 10 μg/mL) at different time points. (A) Anti-proliferative effect of α-mangostin in BGC-823 gastric adenocarcinoma cells; (B) Anti-proliferative effect of α-mangostin in SGC-7901 gastric adenocarcinoma cells. The results are representative of three independent experiments. bP<0.05 vs untreated group.
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fig1: Anti-proliferative effect of α-mangostin (0 to 10 μg/mL) at different time points. (A) Anti-proliferative effect of α-mangostin in BGC-823 gastric adenocarcinoma cells; (B) Anti-proliferative effect of α-mangostin in SGC-7901 gastric adenocarcinoma cells. The results are representative of three independent experiments. bP<0.05 vs untreated group.

Mentions: We initially investigated the effect of α-mangostin on the proliferation of BGC-823 and SGC-7901 cells using the MTT assay. Both gastric adenocarcinoma cell lines were treated with graded concentrations of α-mangostin (0 to 10 μg/mL) for 6, 12, 18, 24, and 48 h. As shown in Figure 1A, cell proliferation was inhibited by α-mangostin treatment in a time- and concentration-dependent manner. Compared with 0 μg/mL (DMSO treatment alone), cell proliferation was not significantly altered at a concentration of α-mangostin (≤3 μg/mL), indicating that α-mangostin is not toxic to BGC-823 cells at these dosages. When cells were treated with 5 to 10 μg/mL, cell viability was significantly decreased. The same result was observed in SGC-7901 cells, although these cells were less sensitive to the cytotoxic effect of α-mangostin than the BGC-823 cells (Figure 1B). Thus, α-mangostin induces potent growth inhibition in gastric adenocarcinoma cells. The optimal concentration 7 μg/mL of α-mangostin was therefore used for subsequent experiments.


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)

Anti-proliferative effect of α-mangostin (0 to 10 μg/mL) at different time points. (A) Anti-proliferative effect of α-mangostin in BGC-823 gastric adenocarcinoma cells; (B) Anti-proliferative effect of α-mangostin in SGC-7901 gastric adenocarcinoma cells. The results are representative of three independent experiments. bP<0.05 vs untreated group.
© Copyright Policy
Related In: Results  -  Collection

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

fig1: Anti-proliferative effect of α-mangostin (0 to 10 μg/mL) at different time points. (A) Anti-proliferative effect of α-mangostin in BGC-823 gastric adenocarcinoma cells; (B) Anti-proliferative effect of α-mangostin in SGC-7901 gastric adenocarcinoma cells. The results are representative of three independent experiments. bP<0.05 vs untreated group.
Mentions: We initially investigated the effect of α-mangostin on the proliferation of BGC-823 and SGC-7901 cells using the MTT assay. Both gastric adenocarcinoma cell lines were treated with graded concentrations of α-mangostin (0 to 10 μg/mL) for 6, 12, 18, 24, and 48 h. As shown in Figure 1A, cell proliferation was inhibited by α-mangostin treatment in a time- and concentration-dependent manner. Compared with 0 μg/mL (DMSO treatment alone), cell proliferation was not significantly altered at a concentration of α-mangostin (≤3 μg/mL), indicating that α-mangostin is not toxic to BGC-823 cells at these dosages. When cells were treated with 5 to 10 μg/mL, cell viability was significantly decreased. The same result was observed in SGC-7901 cells, although these cells were less sensitive to the cytotoxic effect of α-mangostin than the BGC-823 cells (Figure 1B). Thus, α-mangostin induces potent growth inhibition in gastric adenocarcinoma cells. The optimal concentration 7 μg/mL of α-mangostin was therefore used for subsequent experiments.

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