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Anti-Tumor Effect of Pinus massoniana Bark Proanthocyanidins on Ovarian Cancer through Induction of Cell Apoptosis and Inhibition of Cell Migration.

Liu J, Bai J, Jiang G, Li X, Wang J, Wu D, Owusu L, Zhang E, Li W - PLoS ONE (2015)

Bottom Line: Pinus massoniana bark proanthocyanidins (PMBPs), an active component isolated from Pinus massoniana bark, has been reported to possess a wide range of biochemical properties.The underlying mechanisms involved were elucidated to include the loss of mitochondrial membrane potential, down-regulation of the anti-apoptotic protein Bcl-2 and the activation of Caspase 3/9, suggesting that PMBPs triggered apoptosis through activation of mitochondria-associated apoptotic pathway.PMBPs dramatically inhibited MMP-9 activity and expression, blocked the activity of NFκB and the activation of ERK1/2 and p38 MAPK.

View Article: PubMed Central - PubMed

Affiliation: Department of Biotechnology, Dalian Medical University, Dalian, Liaoning, China.

ABSTRACT
Pinus massoniana bark proanthocyanidins (PMBPs), an active component isolated from Pinus massoniana bark, has been reported to possess a wide range of biochemical properties. Here, we investigated the anti-tumor effect of PMBPs on ovarian cancer. The results indicated that PMBPs significantly reduced the growth of ovarian cancer cells and induced dose-dependent apoptosis. The underlying mechanisms involved were elucidated to include the loss of mitochondrial membrane potential, down-regulation of the anti-apoptotic protein Bcl-2 and the activation of Caspase 3/9, suggesting that PMBPs triggered apoptosis through activation of mitochondria-associated apoptotic pathway. In addition, wound healing and transwell chamber assays revealed that PMBPs could suppress migration and invasion of ovarian cancer cells. PMBPs dramatically inhibited MMP-9 activity and expression, blocked the activity of NFκB and the activation of ERK1/2 and p38 MAPK. Our findings suggest that PMBPs has the potential to be developed as an anti-tumor drug for ovarian cancer treatment and/ or disease management.

No MeSH data available.


Related in: MedlinePlus

PMBPs impaired the migration and invasion of ovarian cancer cells as assessed by transwell chamber assay.A2780 and OV2008 cells were treated with PMBPs (0, 5, 10, 25 μg/ml) for 24 h. (A) Representative images of cells that migrated and invaded onto the underside of transwell membrane at 100× magnification under a microscope. (B,C) Number of cells of each field was counted and averaged. Invaded cells were expressed relative to that of control group. The experiments were repeated three times. **P<0.01 and ***P<0.001 compared to the control group.
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pone.0142157.g006: PMBPs impaired the migration and invasion of ovarian cancer cells as assessed by transwell chamber assay.A2780 and OV2008 cells were treated with PMBPs (0, 5, 10, 25 μg/ml) for 24 h. (A) Representative images of cells that migrated and invaded onto the underside of transwell membrane at 100× magnification under a microscope. (B,C) Number of cells of each field was counted and averaged. Invaded cells were expressed relative to that of control group. The experiments were repeated three times. **P<0.01 and ***P<0.001 compared to the control group.

Mentions: Cell migration and invasion are hallmarks of tumor cells. To investigate whether PMBPs impaired migration and invasion of ovarian cancer cells, we performed wound healing assay with different, not apoptotic (5 μg/ml and 10 μg/ml), concentrations of PMBPs for 24 h. We found that PMBPs dose-dependently decreased the movement of A2780 and OV2008 cells (Fig 5). The wound closure rates of PMBPs treated cells were lower than that of non-treated cells (P<0.01) (Fig 5B and 5C). Additionally, we examined the invasiveness of these cells using a 24-well transwell chamber in the presence of different concentrations of PMBPs for 24 h. PMBPs significantly inhibited the migration and invasion potential of the ovarian cancer cells in a dose-dependent manner (P<0.01) (Fig 6). Treatment with 5–25 μg/ml PMBPs inhibited migration and invasion by 27%-66%, respectively, in A2780 cells, and 11%-40% in OV2008 cells, compared to controls (Fig 6B and 6C). Both wound healing assay and transwell chamber assay suggest that PMBPs could suppress the migration and invasion of ovarian cancer cells.


Anti-Tumor Effect of Pinus massoniana Bark Proanthocyanidins on Ovarian Cancer through Induction of Cell Apoptosis and Inhibition of Cell Migration.

Liu J, Bai J, Jiang G, Li X, Wang J, Wu D, Owusu L, Zhang E, Li W - PLoS ONE (2015)

PMBPs impaired the migration and invasion of ovarian cancer cells as assessed by transwell chamber assay.A2780 and OV2008 cells were treated with PMBPs (0, 5, 10, 25 μg/ml) for 24 h. (A) Representative images of cells that migrated and invaded onto the underside of transwell membrane at 100× magnification under a microscope. (B,C) Number of cells of each field was counted and averaged. Invaded cells were expressed relative to that of control group. The experiments were repeated three times. **P<0.01 and ***P<0.001 compared to the control group.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4634942&req=5

pone.0142157.g006: PMBPs impaired the migration and invasion of ovarian cancer cells as assessed by transwell chamber assay.A2780 and OV2008 cells were treated with PMBPs (0, 5, 10, 25 μg/ml) for 24 h. (A) Representative images of cells that migrated and invaded onto the underside of transwell membrane at 100× magnification under a microscope. (B,C) Number of cells of each field was counted and averaged. Invaded cells were expressed relative to that of control group. The experiments were repeated three times. **P<0.01 and ***P<0.001 compared to the control group.
Mentions: Cell migration and invasion are hallmarks of tumor cells. To investigate whether PMBPs impaired migration and invasion of ovarian cancer cells, we performed wound healing assay with different, not apoptotic (5 μg/ml and 10 μg/ml), concentrations of PMBPs for 24 h. We found that PMBPs dose-dependently decreased the movement of A2780 and OV2008 cells (Fig 5). The wound closure rates of PMBPs treated cells were lower than that of non-treated cells (P<0.01) (Fig 5B and 5C). Additionally, we examined the invasiveness of these cells using a 24-well transwell chamber in the presence of different concentrations of PMBPs for 24 h. PMBPs significantly inhibited the migration and invasion potential of the ovarian cancer cells in a dose-dependent manner (P<0.01) (Fig 6). Treatment with 5–25 μg/ml PMBPs inhibited migration and invasion by 27%-66%, respectively, in A2780 cells, and 11%-40% in OV2008 cells, compared to controls (Fig 6B and 6C). Both wound healing assay and transwell chamber assay suggest that PMBPs could suppress the migration and invasion of ovarian cancer cells.

Bottom Line: Pinus massoniana bark proanthocyanidins (PMBPs), an active component isolated from Pinus massoniana bark, has been reported to possess a wide range of biochemical properties.The underlying mechanisms involved were elucidated to include the loss of mitochondrial membrane potential, down-regulation of the anti-apoptotic protein Bcl-2 and the activation of Caspase 3/9, suggesting that PMBPs triggered apoptosis through activation of mitochondria-associated apoptotic pathway.PMBPs dramatically inhibited MMP-9 activity and expression, blocked the activity of NFκB and the activation of ERK1/2 and p38 MAPK.

View Article: PubMed Central - PubMed

Affiliation: Department of Biotechnology, Dalian Medical University, Dalian, Liaoning, China.

ABSTRACT
Pinus massoniana bark proanthocyanidins (PMBPs), an active component isolated from Pinus massoniana bark, has been reported to possess a wide range of biochemical properties. Here, we investigated the anti-tumor effect of PMBPs on ovarian cancer. The results indicated that PMBPs significantly reduced the growth of ovarian cancer cells and induced dose-dependent apoptosis. The underlying mechanisms involved were elucidated to include the loss of mitochondrial membrane potential, down-regulation of the anti-apoptotic protein Bcl-2 and the activation of Caspase 3/9, suggesting that PMBPs triggered apoptosis through activation of mitochondria-associated apoptotic pathway. In addition, wound healing and transwell chamber assays revealed that PMBPs could suppress migration and invasion of ovarian cancer cells. PMBPs dramatically inhibited MMP-9 activity and expression, blocked the activity of NFκB and the activation of ERK1/2 and p38 MAPK. Our findings suggest that PMBPs has the potential to be developed as an anti-tumor drug for ovarian cancer treatment and/ or disease management.

No MeSH data available.


Related in: MedlinePlus