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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, B) Immunodetection of Stat3 and pStat3 protein in gastric adenocarcinoma cells. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL). After 24 h, fluorescent imaging was obtained with a confocal laser scanning microscope. The pSTAT3 fluorescence signal in α-mangostin group was lower than the control group, whereas the STAT3 fluorescence signal was not different between groups. (C, D) Western blot analyses of STAT3, p-STAT3. (E, F) Quantification of Western blot data. Data are representative of three independent assays. bP<0.05 vs control.
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fig4: (A, B) Immunodetection of Stat3 and pStat3 protein in gastric adenocarcinoma cells. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL). After 24 h, fluorescent imaging was obtained with a confocal laser scanning microscope. The pSTAT3 fluorescence signal in α-mangostin group was lower than the control group, whereas the STAT3 fluorescence signal was not different between groups. (C, D) Western blot analyses of STAT3, p-STAT3. (E, F) Quantification of Western blot data. Data are representative of three independent assays. bP<0.05 vs control.

Mentions: To understand the molecular mechanisms underlying α-mangostin-induced gastric adenocarcinoma cell apoptosis, an immunofluorescence assay was performed to determine STAT3 and pSTAT3 alterations in SGC-7901 and BGC-823 cells treated with α-mangostin and stained with TRITC. The cells were also analysed by confocal microscopy. After 24 h, the pSTAT3 fluorescence signal in the α-mangostin group was lower than that in the control group, whereas no difference was observed between two groups in terms of STAT3 expression (Figures 4A, 4B). To confirm pSTAT3 alteration further, we performed a sequential test using Western blot analysis. The results were in agreement with those of the immunofluorescence assay (Figures 4C–4F). These findings further indicate that the STAT3 signaling pathway is involved in the anti-tumor effects of α-mangostin.


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, B) Immunodetection of Stat3 and pStat3 protein in gastric adenocarcinoma cells. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL). After 24 h, fluorescent imaging was obtained with a confocal laser scanning microscope. The pSTAT3 fluorescence signal in α-mangostin group was lower than the control group, whereas the STAT3 fluorescence signal was not different between groups. (C, D) Western blot analyses of STAT3, p-STAT3. (E, F) Quantification of Western blot 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

fig4: (A, B) Immunodetection of Stat3 and pStat3 protein in gastric adenocarcinoma cells. BGC-823 and SGC-7901 cells were incubated with α-mangostin (7 μg/mL). After 24 h, fluorescent imaging was obtained with a confocal laser scanning microscope. The pSTAT3 fluorescence signal in α-mangostin group was lower than the control group, whereas the STAT3 fluorescence signal was not different between groups. (C, D) Western blot analyses of STAT3, p-STAT3. (E, F) Quantification of Western blot data. Data are representative of three independent assays. bP<0.05 vs control.
Mentions: To understand the molecular mechanisms underlying α-mangostin-induced gastric adenocarcinoma cell apoptosis, an immunofluorescence assay was performed to determine STAT3 and pSTAT3 alterations in SGC-7901 and BGC-823 cells treated with α-mangostin and stained with TRITC. The cells were also analysed by confocal microscopy. After 24 h, the pSTAT3 fluorescence signal in the α-mangostin group was lower than that in the control group, whereas no difference was observed between two groups in terms of STAT3 expression (Figures 4A, 4B). To confirm pSTAT3 alteration further, we performed a sequential test using Western blot analysis. The results were in agreement with those of the immunofluorescence assay (Figures 4C–4F). These findings further indicate that the STAT3 signaling pathway is involved in the anti-tumor effects of α-mangostin.

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