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Endometriosis (EM) is a chronic, estrogen-dependent inflammatory disease. Presently, the pathophysiology of EM is still unclear, and numerous studies have established that the immune system plays a major role in the pathophysiology of EM. Six microarray datasets were downloaded from the GEO public database. A total of 151 endometrial samples (72 ectopic endometria and 79 controls) were included in this study. CIBERSORT and ssGSEA were applied to calculate the immune infiltration of EM and control samples. Moreover, we validated four different correlation analyses to explore immune microenvironment of EM and finally identified M2 macrophage-related hub genes and further conducted the specific immunologic signaling pathway analysis by GSEA. The logistic regression model was investigated by ROC and further validated by two external datasets. From the results of the two immune infiltration assays, we concluded that M2 macrophages, regulatory T cells (Tregs), M1 macrophages, activated B cells, T follicular helper cells, activated dendritic cells, and resting NK cells have a significant difference between control and EM tissues. Through multidimensional correlation analysis, we found that macrophages play an important central role in cell-to-cell interactions, especially M2 macrophages. Four immune-related hub genes, namely FN1, CCL2, ESR1, and OCLN, are closely related to M2 macrophages and play a crucial role in the occurrence and immune microenvironment of endometriosis. The combined AUC of ROC prediction model in test and validation sets were 0.9815 and 0.8206, respectively. We conclude that M2 macrophages play a central role in the immune-infiltrating microenvironment of EM.

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Background: There has been lack of guidance for stratify treatment between cervical endometrioid adenocarcinoma (EC) and ordinary cervical adenocarcinoma (AC), therefore understanding the difference of prognosis between EC and AC is important for individualized therapy for these patients. Methods: In this study, we compare the survival outcomes between cervical EC and AC patients from the SEER database. we analyzed 2,554 patients for overall survival (OS) and 2,527 patients for disease-specific survival (DSS), Cox regression and Kaplan-Meier analyses were conducted to analyze the survival outcomes of the AC and EC patients, a 1:1 propensity score matching (PSM) method was used to match patients and balance various factors, OS and DSS were analyzed among the subgroups before and after 1:1 PSM. Results: In the unmatched cohort, in the multivariate analysis, no statistically significant difference was found in terms of OS (P=0.24) and DSS (P=0.20) between the EC and AC patients, The 3- and 5-year OS rates were 77.89% and 72.65% for the AC patients, and 83.38% and 75.64% for the EC patients respectively. The 3- and 5-year DSS rates were 84.93% and 79.69% for the EC patients, 83.97% and 76.78% for the AC patients, respectively. In the PSM cohort, 280 AC patients and 280 EC patients were included in the analysis of OS. 273 AC patients and 275 EC patients were included in the analysis of DSS, the Kaplan-Meier analysis and the multivariate analysis also produced similar results for the unmatched groups. Conclusions: There were no statistically significant differences in OS and DSS between the cervical EC and AC patients.

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CD44 is a prognostic indicator of shorter survival time in ovarian cancer. E-cadherin fragmentation promotes the progression of ovarian cancer. However, the effects of CD44 and E-cadherin overexpression on ovarian cancer cells have remained elusive. The present study aimed to investigate the effects of overexpression of CD44 and E-cadherin on cell proliferation, adhesion and invasion of SKOV-3 and OVCAR-3 ovarian cancer cells. Overexpression of CD44 and E-cadherin was achieved by transfecting SKOV-3 and OVCAR-3 cells with viruses carrying the CD44 or E-cadherin gene, respectively. Expression of CD44 and E-cadherin was detected by western blot analysis. The proliferation of SKOV-3 and OVCAR-3 cells was measured by a Cell Counting Kit-8 at 0, 24 and 48 h after viral transfection. The adhesion ability of SKOV-3 and OVCAR-3 cells to the endothelial layer was detected. A Transwell invasion assay was utilized to assess the invasion ability of the cells. Overexpression of CD44 and E-cadherin in SKOV-3 and OVCAR-3 cells was confirmed by western blot. Compared with the blank or negative control groups, the CD44 overexpression groups of SKOV-3 and OVCAR-3 cells exhibited an increased cell proliferation rate at 24 and 48 h, whereas overexpression of E-cadherin did not alter the proliferation of these cells. Furthermore, compared with the blank and negative control groups, the cell adhesion and invasion ability in the CD44 overexpression groups of SKOV-3 and OVCAR-3 cells was markedly higher. There were no significant differences in adhesion ability between the E-cadherin overexpression group and the blank/negative control group. Of note, overexpression of E-cadherin decreased the invasive ability of SKOV-3 and OVCAR-3 cells. In conclusion, Overexpression of CD44 increased the proliferation, adhesion and invasion of ovarian cancer cells, while overexpression of E-cadherin decreased the invasion of ovarian cancer cells.

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Ovarian cancer is the most common cause of gynecological cancer-related mortality. Serine/threonine protein phosphatase 5 (PP5, PPP5C) has been recognized to be involved in the regulation of multiple cellular signaling cascades that control diverse cellular processes, including cell growth, differentiation, proliferation, motility and apoptosis. In this study, to evaluate the functional role of PP5 in ovarian cancer cells, lentivirus-mediated RNA interference (RNAi) was applied to silence PPP5C in the human ovarian cancer cell line CAOV-3. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell colony forming ability was measured by colony formation. Cell cycle progression was determined by propidium iodide staining and flow cytometry. The results demonstrated that lentivirus-mediated RNAi specifically suppressed the expression of PPP5C at the mRNA and protein levels in CAOV-3 cells. Further investigations revealed that PP5 knockdown significantly inhibited the proliferation and colony formation of CAOV-3 cells. Moreover, the cell cycle of CAOV-3 cells was arrested at the G0/G1 phase following PP5 knockdown. This study highlights the crucial role of PP5 in promoting ovarian cancer cell proliferation, and provides a foundation for further study into the clinical potential of lentiviral-mediated delivery of PP5 RNAi therapy for the treatment of ovarian cancer.

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OBJECTIVE: To compare the efficacy and safety profile of carbetocin with other uterotonic agents in preventing postpartum hemorrhage. METHODS: PubMed, Web of Science, Scopus and EBSCOhost were searched for relevant randomized controlled trials published until September 2013. RESULTS: Carbetocin was associated with a significantly reduced need for additional uterotonic agents (RR = 0.68, 95% CI: 0.55-0.84, I(2 )= 4%) compared with oxytocin in women following cesarean delivery. However, with respect to postpartum hemorrhage, severe postpartum hemorrhage, mean estimated blood loss and adverse effects, our analysis failed to detect a significant difference. Studies comparing carbetocin with syntometrine in women undergoing vaginal delivery demonstrated no statistical difference in terms of risk of postpartum hemorrhage, severe postpartum hemorrhage or the need for additional uterotonic agents, but the risk of adverse effect was significantly lower in the carbetocin group. CONCLUSIONS: Carbetocin has been associated with a similar low incidence of adverse effects to oxytocin and at least as effective as syntometrine and may become an alternative uterotonic agent for the prevention of postpartum hemorrhage. Further studies should be conducted to determine the safety and efficacy profile of carbetocin in women with cardiac disorders and to analyze the cost-effectiveness and minimum effective dose of carbetocin.

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