Alkaline fermentation of refinery waste activated sludge mediated by refinery spent caustic for volatile fatty acids production.

Volatile fatty acids (VFA), produced from waste activated sludge (WAS), provide unique opportunities for resource recovery in wastewater treatment plants. This study investigates the potential of refinery spent caustic (RSC) on VFA production during refinery WAS (RWAS) alkaline fermentation. The highest VFA yield was 196.3 mg/g-VS at a sludge retention time of 6 days. Amplicon sequencing revealed the enrichment of Soehngenia (20.21%), Bacilli (11.86%), and Brassicibacter (4.17%), which was associated with improved activities of protease (626%) and α-glucosidase (715%). Function prediction analysis confirmed that acetyl-CoA production and fatty acid biosynthesis were enhanced, while fatty acid degradation was inhibited. Accordingly, hydrolysis, acidogenesis, and acetogenesis were improved by 6.87%, 10.67%, and 28.50%, respectively; whereas methanogenesis was inhibited by 28.87%. The sulfate and free ammonia in RSC likely contributed to increased acetic acid production. This study showcases that RWAS alkaline fermentation mediated by RSC for VFA production is the practicable approach.

The epithelial-mesenchymal transition of glioma cells promotes tissue factor expression via the miR200a/ZEB1 axis.

Glioma is the most common brain tumor and the main cause of death from primary brain tumors. Due to the limitations of current diagnostic and treatment methods, the prognosis of high-grade glioma is not optimistic and is prone to venous thrombosis. Epithelial-mesenchymal transition (EMT) is a vital step for glioma cells to obtain a highly migratory and invasive cell phenotype. Tissue factor (TF) is the downstream target of several carcinogenic pathways. According to reports, the TF gene is highly methylated and down-regulated in IDH1 mutant gliomas with good prognosis. We aimed to investigate the impact of EMT on the expression of TF in glioma cells, as well as the corresponding mechanism. Our data indicated that the expression level of TF in glioma tissues increased, and was positively correlated with the WHO classification of glioma. After inducing EMT in glioma cells in vitro, TF expression increased significantly, indicating that EMT in glioma cells can promote TF expression. Further studies have shown that the expression level of ZEB1 is positively correlated with the WHO classification of glioma tissues and the expression level of TF in glioma tissues. This study proved that EMT promotes the expression of TF in glioma cells through the miR-200a/ZEB1 axis. In summary, these results indicated that EMT can promote the expression of TF in glioma cells via the miR-200a/ZEB1 axis. For gliomas, TF is related to EMT and has the potential to become an effective target against EMT and thrombotic events.

Nitidine chloride suppresses epithelial-mesenchymal transition and stem cell-like properties in glioblastoma by regulating JAK2/STAT3 signaling.

Glioblastoma is the most aggressive and common intracranial malignant tumor, and the prognosis is still poor after various treatments. Based on the poor prognosis of glioma, new drugs that suppress the rapid progression and aggressive growth of glioma are urgently needed. It has been reported that nitidine chloride (NC) can inhibit tumor growth and epithelial-mesenchymal transition (EMT), and EMT is associated with cancer stem cell properties. The present study aimed to investigate the inhibitory effect of NC on the EMT process and stem cell-like properties in glioma cells. The results showed that the migration and invasion abilities in U87 and LN18 glioma cells were significantly increased after the induction of EMT and these effects were inhibited by NC in a concentration-dependent manner. NC treatment decreased the expression of EMT markers in glioma cells and self-renewal capacity of glioma stem-like cells. We demonstrated that these effects of NC were achieved via JAK2/STAT3 signaling. Taken together, these results indicate that NC inhibits the EMT process and glioma stem-like properties via JAK2/STAT3 signaling pathway, suggesting that NC may be a potential anti-glioma drug.