Microbial co-occurrence networks driven by low-abundance microbial taxa during composting dominate lignocellulose degradation.

Lignocellulose, which contains cellulose, hemicellulose and lignin, is one of the most important factors determining the rate and quality of compost decomposition, and the microbial community composition affects the rate of lignocellulose decomposition. Interactions between microbial taxa contribute significantly to ecosystem energy flow and material cycling. However, it is not clear how interactions between microbial taxa affect the degradation of lignocellulose during the composting process. For this reason we carried out aerobic co-composting experiments with maize straw and cattle manure to explore the contribution of microbial community diversity and the interaction between taxa to lignocellulosic degradation. The results showed that moisture and temperature had the greatest effect on microbial communities during composting and that lignocellulose degradation was dominated by microbial co-occurrence networks rather than microbial community diversity. Overall co-occurrence network and bacterial-fungal interactions explained 23.9-84.1 % of lignocellulosic degradation, whereas microbial diversity only accounted for 24.6-31.5 %. Interestingly, keystone taxa analysis of the microbial co-occurrence networks revealed that low-abundance taxa influenced microbial interactions driving lignocellulose degradation. Our results provide a new perspective for understanding lignocellulose degradation during composting, offering insights into important microbial interaction mechanisms for improving compost quality and efficiency.

Mithramycin inhibits epithelial-to-mesenchymal transition and invasion by downregulating SP1 and SNAI1 in salivary adenoid cystic carcinoma.

Mithramycin exhibits certain anticancer effects in glioma, metastatic cerebral carcinoma, malignant lymphoma, chorionic carcinoma and breast cancer. However, its effects on salivary adenoid cystic carcinoma remain unclear. Here, we report that mithramycin significantly inhibited epithelial-to-mesenchymal transition and invasion in human salivary adenoid cystic carcinoma cell lines. The underlying mechanism for this activity was further demonstrated to involve decreasing the expression of the transcription factors specificity protein 1 and SNAI1. Specificity protein 1 is a pro-tumourigenic transcription factor that is overexpressed in SACC-LM and SACC-83 cells, and its expression is inhibited by mithramycin. Moreover, chromatin immunoprecipitation assays showed that specificity protein 1 induced SNAI1 transcription through direct binding to the SNAI1 promoter. In summary, this study uncovered the mechanism through which mithramycin inhibits epithelial-to-mesenchymal transition and invasion in salivary adenoid cystic carcinoma cell lines, namely, via downregulating specificity protein 1 and SNAI1 expression, which suggests mithramycin may be a promising therapeutic option for salivary adenoid cystic carcinoma.