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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

Alpha-mangostin blocks Bcl-xL and Mcl-1 expression in gastric adenocarcinoma cells. BGC-823 (A) and SGC-7901 (B) cells were treated with or without α-mangostin (7 μg/mL) for 6, 18, and 24 h, from which lysates were prepared. Western blot analyses of cell lysates probed for Bcl-xL and Mcl-1. (C, D) Quantification of Western blotting data. Data are representative of three independent assays. bP<0.05 vs control.
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fig5: Alpha-mangostin blocks Bcl-xL and Mcl-1 expression in gastric adenocarcinoma cells. BGC-823 (A) and SGC-7901 (B) cells were treated with or without α-mangostin (7 μg/mL) for 6, 18, and 24 h, from which lysates were prepared. Western blot analyses of cell lysates probed for Bcl-xL and Mcl-1. (C, D) Quantification of Western blotting data. Data are representative of three independent assays. bP<0.05 vs control.

Mentions: To elucidate further the mechanism by which α-mangostin-mediated inhibition of constitutive Stat3 activation results in cell growth inhibition and apoptosis, we examined the anti-apoptotic proteins, Bcl-xL and Mcl-1, both of which are target genes for Stat3. Using SGC-7901 and BGC-823 cells treated with α-mangostin, Western blot analysis showed significant reductions in the levels of expression of Bcl-xL and Mcl-1 (Figure 5), which correlates with the inhibition of Stat3 phosphorylation and activity by α-mangostin (Figure 4). These data suggest that α-mangostin induces cell growth inhibition and apoptosis of tumor cells, at least in part, by inhibiting Stat3-depedent induction of Bcl-xL and Mcl-1.


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)

Alpha-mangostin blocks Bcl-xL and Mcl-1 expression in gastric adenocarcinoma cells. BGC-823 (A) and SGC-7901 (B) cells were treated with or without α-mangostin (7 μg/mL) for 6, 18, and 24 h, from which lysates were prepared. Western blot analyses of cell lysates probed for Bcl-xL and Mcl-1. (C, D) Quantification of Western blotting data. Data are representative of three independent assays. bP<0.05 vs control.
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Related In: Results  -  Collection

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

fig5: Alpha-mangostin blocks Bcl-xL and Mcl-1 expression in gastric adenocarcinoma cells. BGC-823 (A) and SGC-7901 (B) cells were treated with or without α-mangostin (7 μg/mL) for 6, 18, and 24 h, from which lysates were prepared. Western blot analyses of cell lysates probed for Bcl-xL and Mcl-1. (C, D) Quantification of Western blotting data. Data are representative of three independent assays. bP<0.05 vs control.
Mentions: To elucidate further the mechanism by which α-mangostin-mediated inhibition of constitutive Stat3 activation results in cell growth inhibition and apoptosis, we examined the anti-apoptotic proteins, Bcl-xL and Mcl-1, both of which are target genes for Stat3. Using SGC-7901 and BGC-823 cells treated with α-mangostin, Western blot analysis showed significant reductions in the levels of expression of Bcl-xL and Mcl-1 (Figure 5), which correlates with the inhibition of Stat3 phosphorylation and activity by α-mangostin (Figure 4). These data suggest that α-mangostin induces cell growth inhibition and apoptosis of tumor cells, at least in part, by inhibiting Stat3-depedent induction of Bcl-xL and Mcl-1.

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