An integrated analysis of dysregulated SCD1 in human cancers and functional verification of miR-181a-5p/SCD1 axis in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC), one of the most lethal cancers, has become a global health issue. Stearoyl-coA desaturase 1 (SCD1) has been demonstrated to play a crucial role in human cancers. However, pan-cancer analysis has revealed little evidence to date. In the current study, we systematically inspected the expression patterns and potential clinical outcomes of SCD1 in multiple human cancers. SCD1 was dysregulated in several types of cancers, and its aberrant expression acted as a diagnostic biomarker, indicating that SCD1 may play a role in tumorigenesis. We used ESCC as an example to demonstrate that SCD1 was dramatically upregulated in tumor tissues of ESCC and was associated with clinicopathological characteristics in ESCC patients. Furthermore, Kaplan-Meier analysis showed that high SCD1 expression was correlated with poor progression-free survival (PFS) and disease-free survival (DFS) in ESCC patients. The protein-protein interaction (PPI) network and module analysis by PINA database and Gephi were performed to identify the hub targets. Meanwhile, the functional annotation analysis of these hubs was constructed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Functionally, the gain-of-function of SCD1 in ESCC cells promoted cell proliferation, migration, and invasion; in contrast, loss-of-function of SCD1 in ESCC cells had opposite effects. Bioinformatic, QPCR, Western blotting and luciferase assays indicated that SCD1 was a direct target of miR-181a-5p in ESCC cells. In addition, gain-of-function of miR-181a-5p in ESCC cells reduced the cell growth, migratory, and invasive abilities. Conversely, inhibition of miR-181a-5p expression by its inhibitor in ESCC cells had opposite biological effects. Importantly, reinforced SCD1 in miR-181a-5p mimic ESCC transfectants reversed miR-181a-5p mimic-prevented malignant phenotypes of ESCC cells. Taken together, these results indicate that SCD1 expression influences tumor progression in a variety of cancers, and the miR-181a-5p/SCD1 axis may be a potential therapeutic target for ESCC treatment.

Metagenomic analysis of microbial community and metabolic pathway of simultaneous sulfide and nitrite removal process exposed to divergent hydraulic retention times.

The role of hydraulic retention time (HRT) on S0 production was assessed through metagenomics analyses. Considering comprehensive performance for the tested HRTs (0.25-13.33 h), the optimal HRT was 1 h, while respective sulfide and nitrite loading rate could reach 6.84 kg S/(m3·d) and 1.95 kg N/(m3·d), and total S0 yield was 0.36 kg S/(kg (VSS)·d). Bacterial community richness decreased along the shortening of HRT. Microbacterium, Sulfurimonas, Sulfurovum, Paracoccus and Thauera were highly abundant bacteria. During sulfur metabolism, high expression of sqr gene was the main reason of maintaining high desulfurization load, while lacking soxB caused the continuous increase of S0. Regarding nitrogen metabolism, the rapid decrease of nitrite transporter prevented nitrite to enter in cells, which caused a rapid decrease of nitrite removal under extreme HRT. Adjusting HRT is an effective way to enhance S0 production for the application of the simultaneous sulfide and nitrite removal process.