BackgroundTo determine the expression of bone morphogenetic protein-2 (BMP-2) and its receptors BMPRIA, BMPRIB, and BMPRII in epithelial ovarian cancer (EOC) and to analyze their influence on the prognosis of ovarian cancer patients.MethodsSemi-quantitative RT-PCR and western blot were applied to detect the expression of BMP-2 and its receptors BMPRIA, BMPRIB, and BMPRII in EOC, benign ovarian tumors, and normal ovarian tissue at the mRNA and protein levels. Immunohistochemistry was used to determine the expression of BMP-2 and its receptors in 100 patients with EOC to analyze their influence on the five-year survival rate and survival time of ovarian cancer patients.Results(1) The mRNA and protein expression levels of BMP-2, BMPRIB, and BMPRII in ovarian cancer tissue were remarkably lower than those in benign ovarian tumors and normal ovarian tissue, while no significant differences in BMPRIA expression level was found among the three kinds of tissues. (2) The five-year survival rate and the average survival time after surgery of EOC patients with positive expression of BMP-2, BMPRIB, and BMPRII were remarkably higher than those of patients with negative expression of BMP-2, BMPRIB, and BMPRII. BMPRIA expression was not associated with the five-year survival rate or with the average survival time of ovarian cancer patients.ConclusionsBMP-2, BMPRIB, and BMPRII exhibited low expression in EOC tissue, and variation or loss of expression may indicate poor prognosis for ovarian cancer patients.

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Our study highlighted a pivotal role for PLGF in prevention and treatment of GDM in patients with PE.

Background/Aim: Reduction in serum placental growth factor (PLGF) frequently co-occurs with preeclampsia (PE) and gestational diabetes mellitus (GDM). Recently, we reported that impairment in gestational beta-cell mass growth may result from PE-associated reduction in PLGF and lead to development of GDM. Here, we studied the underlying mechanisms. Methods: We co-cultured primary mouse beta cells with mouse islet endothelial cells (MS1), with or without PLGF. We also cultured beta cells in conditioned media from PLGF-treated MS1. Specific signal-pathway inhibitors were applied to cultured beta cells in conditioned media from PLGF-treated MS1. We analysed beta-cell proliferation by BrdU incorporation. We analysed changes in cell number by a MTT assay. We analysed protein levels of cell-cycle regulators in beta cells by Western blot. Results: PLGF itself failed to induce beta-cell proliferation, but significantly augmented proliferation of beta cells co-cultured with MS1, which resulted in significant increases in cell number. Conditioned media from the PLGF-treated MS1 cells similarly induced beta-cell proliferation, which was abolished by inhibition of PI3k/Akt signalling, but not by inhibition of either ERK/MAPK or JNK signalling. The induction of beta-cell proliferation by PLGF-treated MS1 cells appeared to involve decreases in cell-cycle inhibitors p21 and p27, and increases in cell-cycle activators CDK4 and CyclinD1. Conclusion: Gestational PLGF may target islet endothelial cells to release growth factors that activate PI3k/Akt signalling in beta cells to increase their proliferation. PE-associated reduction in PLGF impairs these processes to result in GDM.

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