Long noncoding RNAs (lncRNAs) have been reported to be involved in various cellular processes and to participate in a variety of human diseases. Recently, increasing studies have reported that lncRNAs are related to many reproductive diseases, such as pathogenesis of recurrent pregnancy loss (RPL), preeclampsia (PE) and gestational diabetes mellitus (GDM). In this study, we aimed to investigate the effect of LINC01088 in trophoblast cells and its potential role in pathogenesis of RPL. LINC01088 was found to be upregulated in first-trimester chorionic villi tissues from RPL patients. Increased LINC01088 repressed proliferation, migration and invasion of trophoblast cells, and promoted apoptosis of trophoblast cells. Further exploration indicated that LINC01088 decreased the production of nitric oxide (NO) by binding and increasing Arginase-1 and decreasing eNOS protein levels. Importantly, JNK and p38 MAPK-signaling pathways were active after overexpression of LINC01088. In conclusion, our studies demonstrated that LINC01088 plays an important role in the pathogenesis of RPL, and is a potential therapeutic target for the treatment of RPL.

Breast Cancer (BC) is the most common cancer in women and the second cause of death in females due to cancers. Most genetic studies point to a significant relationship between Interleukin 10 (IL-10) and BC. IL-10 is strongly expressed in tissues of BC and negatively correlated with the prognosis of several tumors, including breast cancer. In breast cancer cells, the down-regulation of miRNA-141 inhibits IL-10 and contributes to an up-regulation of COX-2, PGE-2, and TNF-α expression. Long non-coding RNR SNHG1 has been increased in CD4 + TIL cells in patients with breast cancer, whereas siRNA-SNHG1 can decrease the expression of Foxp3 and IL-10. Overexpression of IL-10 failed to manage immunogenic cancer. And the inhibition of IL-10Rα improved the therapeutic benefit of chemotherapy in the breast cancer model. The mechanisms of IL-10 in breast cancer are controversial. Interleukin-10 is documented to demonstrate both anti-and pro-tumor acts. IL-10 is strongly expressed in tissues of BC, which has a negative correlation with breast cancer prognosis and tumor marker. Besides, IL10 levels in serum are elevated for patients with BC than normal controls people, which also correlates with poorer outcomes. IL-10 stimulated cancer cell replication and metastasis. IL10 is currently under study as a potential therapeutic targeting inflammatory disease as well as cancer. In conclusion, IL-10 seems to be the future diagnostic biomarker and therapy target of breast cancer. Though lncRNA seems to be a significant research spot, very little research in lncRNA and IL-10 is found. Consequently, in future IL-10 research topics, new studies related to lncRNA could occur.

Pancreatic ductal adenocarcinoma (PDAC) is among the dangerous human cancers, is the 10th highly prevalent cancer, and the fourth sole cause of cancer-related mortality in the United States of America. Notwithstanding the significant commitment, the forecast for people with this burden continues to have a five-year survival rate of just 4–6%. The most critical altered genes within PDAC consist of K-ras the proto-oncogene which is usually mutationally activated above 90% cases and tumor suppressors likeTrp53 are altered at 55%. To face the burden of pancreatic ductal adenocarcinoma, a variety of genetically engineered pancreatic cancer mice models have been created over the last past years. These models have distinctive features and are not all appropriate for preclinical studies. In this review, we focus on differences between two mice models K-rasLSL.G12D/+;Pdx-1-Cre(KC) and K-rasLSL.G12D/+; Trp53R172H/+; Pdx-1-Cre(KPC) in terms of their modeling biology and their clinical relevance.