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The human vaginal microbiota plays essential roles in preventing pathogenic bacteria, fungi, and viruses from invading. The dominant vaginal Lactobacillus species show great potential to be developed as probiotics.

Endometriosis affects 6-10% of healthy women of reproductive age. Therefore, it is important to study the molecular mechanism by which endometriosis develops. This study examined whether aberrant expression of LINC01541 contributes to the pathogenesis of endometriosis. Human endometrial stromal cells (ESCs) were stimulated with 10 nmol/L of 17β-Estradiol (17β-E2) to simulate ectopic cells found in endometriosis. Next, the levels of proteins related to the epithelial-mesenchymal transition (EMT), cell invasion, and metastasis were investigated. The effects of LINCO1541 silencing and overexpression were also examined in ESCs. Cell proliferation and apoptosis were detected by cell counting kit-8 and flow cytometry assays, respectively. ESCs stimulated with 17β-E2 displayed increased levels of N-Cadherin and vimentin expression, but decreased levels of E-Cadherin expression. 17β-E2 promoted the migration and invasion of ESCs, and those affects were partially reversed by overexpression of LINC01541. Furthermore, silencing of LINC01541 attenuated apoptosis and promoted the EMT of ESCs, while overexpression of LINC01541 stimulated cell apoptosis, increased the levels of caspase 3 protein, and decreased the levels of B cell leukemia/lymphoma 2 protein. Overexpression of LINC01541 also decreased the expression of vascular endothelial growth factor A (VEGFA) by repressing the Wnt/β-catenin pathway. Our, results suggest that LINC01541 can inhibit the EMT process, metastasis of ESCs, and VEGFA expression by regulating the Wnt/β-catenin pathway, which may play an important role in the pathogenesis of endometriosis.

A series of macrocyclic analogues were designed and synthesized based on the cocrystal structure of small molecule plasma kallikrein (pKal) inhibitor, 2, with the pKal protease domain. This led to the discovery of a potent macrocyclic pKal inhibitor 29, with an IC50 of 2 nM for one olefinic isomer and 42.3 nM for the other olefinic isomer.

MicroRNAs (miRNAs) are a class of naturally occurring, small, non-coding RNAs that target protein-coding mRNAs at the post-transcriptional level and participate in various biological processes. Our previous studies suggested that miR-143-3p functions as a tumor suppressor and has a role in the progression of ovarian cancer, in part through the regulation of the tumor promoter. In this study, we found that the mRNA expression level of miR-143-3p was significantly decreased in ovarian cancer tissues, in comparison with normal ovarian tissues by high-throughput miRNA profiling and quantitative RT-PCR. Secondly, we indicated that the up-regulation of miR-143-3p in the ovarian cancer cell lines SKOV3, ES2, and OVCAR3 significantly reduced their proliferation, migration, and invasion. Furthermore, miR-143-3p inhibited the growth of ovarian tumors in vivo in a xenograft experiment. In addition, miR-143-3p down-regulated the expression of transforming growth factor (TGF)-β-activated kinase 1 (TAK1) in human ovarian cancer cells. Therefore, our study indicates that miR-143-3p inhibited the proliferation, migration, and invasion of ovarian cancer cells in vitro, as well as ovarian tumorigenesis in vivo. This inhibitory effect may target TAK1, suggesting a potential application of the miR-143-3p-TAK1 pathway in the clinical diagnosis and treatment of ovarian cancer.

MicroRNAs (miRNAs) play important roles in transcriptional regulation by targeting the 3'-UTR of target genes which participate in various biological processes. We aimed to investigate the potential role of miR-28-5p in the process of ovarian cancer development through regulating N4BP1. We found that the mRNA expression level of miR-28-5p was significantly increased in ovarian cancer tissues in comparison with adjacent ovarian tissues by qRT-PCR (P

Ovarian carcinoma is one of the most common and lethal malignancies in the world. Replication factor C (RFC) plays an important role in DNA replication, DNA damage repair, and checkpoint control during cell cycle progression in all eukaryotes. Our previous study found that one unit of RFC complex, RFC3, is over-expressed in ovarian tumor tissues. However, its role in the development of ovarian carcinoma remains unclear. Western blot and real-time RT-PCR analysis were used to measure the expression of RFC3 in ovarian cancer cells. Lentivirus-mediated RFC3-specific shRNA was used to knock down RFC3 expression in ovarian cancer cells. Furthermore, the effect of RFC3 on tumor cellular proliferation and growth were examined, respectively. The expression level of RFC3 was remarkably up-regulated in ovarian cancer OVCAR-3 cells. With MTS and cell growth assays, the viability and proliferation of RFC3 knocking-down OVCAR-3 cell line were shown to be effectively restrained. Down-regulation of RFC3 expression arrested the cell cycle of OVCAR-3 cell in the S-phase and induced apoptosis. This study suggests that RFC3 may play an important role in the the process of ovarian carcinoma, and that it may be a potential biological treatment target in the future.