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. 2010 Jun 24;8:74. doi: 10.1186/1477-7827-8-74

Figure 5.

Figure 5

PAF induced cell proliferation and anti-apoptosis in BRCA1-mutant ovarian epithelial cells. (A) The induced cell proliferation pattern in wild type HOSE-E6E7 and HOSE-27 cells and BRCA1-mutant HOSE-642 and HOSE-636 and ovarian malignant cells (UWB1) was affected by 72 hours treatment with different concentrations of PAF. Significant increase or decrease of cell proliferation induced by PAF treatment was indicated by symbol star (* p < 0.05). (B) Differential cell proliferation pattern was affected by PAF (1 nM) treatment in wild type of HOSE-E6E7 and HOSE-27 cells and BRCA1-mutant non-malignant HOSE-642 and HOSE-636 and ovarian cancer cells (UWB1), compared to the control cells without PAF treatment (as 100%). (C) PAFR-inhibitor, specific PAFR antibody and different concentration of antagonist ginkgolide B (1, 5, 10, 50, 100 μM) significantly (p < 0.05) blocked the PAF-induced proliferation in three BRCA1-mutant ovarian epithelial cell lines, compared to the control cells treated either with equal volume of DMSO or with IgG (as 100%). (D, E) Anti-apoptotic activity was significantly (p < 0.05) induced by PAF treatment in BRCA1-mutant at-risk HOSE-642 cells. (F, G) Apoptosis was significantly induced by PAF (100 nM) in wild-type HOSE-E6E7 cells, compared to the controls with 72 h treatment of equal volume DMSO. Experiments were performed at least three times (p < 0.05).