Novelty three stages for humification of sewage sludge during hyperthermophilic aerobic fermentation.

Compared with conventional aerobic fermentation (CAF), there is limited knowledge of how hyperthermophilic aerobic fermentation (HAF) enhances the humification of sewage sludge. This study compared three novel stages of organic degradation, precursors, functional groups, bacterial community, and humus synthesis mechanism in HAF with CAF. The results showed that organic matter (OM) degraded rapidly, and 68% of the degradation could be completed of stage I in HAF. Compared with the initial stage, ammonium nitrogen (NH4+-N), water-soluble organic carbon, and water-soluble total nitrogen increased by 2.83 times, 40.5 times, and 33.5 times, respectively. Cellulose and hemicellulose decreased by 29.22% and 21.85%, respectively. These results suggested that temperature (>80 °C) and Bacillus dominated accelerate the humification process by rapidly improving OM degradation. Compared with the initial value of HAF, the maximum increment of reducing sugar at stage II was 297%, and the degradation rate of cellulose was effectively increased by 21.03% compared with that of CAF. The precursors such as reducing sugars and amino acids formed humus at stage II. The content of Aryl C increased significantly during the HAF process, the degree of polymerization of humus and the aromatization degree of HA and FA increased significantly, and complex organic macromolecular material polymers were formed at stage III. The sugar-amine condensation was the mechanism of humification in the sludge HAF process. This investigation provided three new stages of insights into the synthesis of humification during the HAF process and extended the current mechanism of humification in the HAF process.

Insight into the role of p62 in the cisplatin resistant mechanisms of ovarian cancer.

Cisplatin is a platinum-based first-line drug for treating ovarian cancer. However, chemotherapy tolerance has limited the efficacy of cisplatin for ovarian cancer patients. Research has demonstrated that cisplatin causes changes in cell survival and death signaling pathways through its interaction with macromolecules and organelles, which indicates that investigation into the DNA off-target effects of cisplatin may provide critical insights into the mechanisms underlying drug resistance. The multifunctional protein p62 works as a signaling hub in the regulation of pro-survival transcriptional factors NF-κB and Nrf2 and connects autophagy and apoptotic signals, which play important roles in maintaining cell homeostasis. In this review, we discuss the role of p62 in cisplatin resistance by exploring p62-associated signaling pathways based on current studies and our work. Insights into these resistance mechanisms may lead to more effective therapeutic strategies for ovarian cancer by targeting p62.

p62 aggregates mediated Caspase 8 activation is responsible for progression of ovarian cancer.

Increasing evidence suggests that p62/SQSTM1 functions as a signalling centre in cancer. However, the role of p62 in tumour development depends on the interacting factors it recruits and its precise regulatory mechanism remains unclear. In this study, we investigated the pro-death signalling recruitment of p62 with the goal of improving anti-tumour drug effects in ovarian cancer treatment. We found that p62 with Caspase 8 high expression is correlated with longer survival time compared with cases of low Caspase 8 expression in ovarian cancer. In vivo experiments suggested that insoluble p62 and ubiquitinated protein accumulation induced by autophagy impairment promoted the activation of Caspase 8 and increased cell sensitivity to cisplatin. Furthermore, p62 functional domain UBA and LIR mutants regulated autophagic flux and attenuated Caspase 8 activation, which indicates that autophagic degradation is involved in p62-mediated activation of Caspase 8 in ovarian cancer cells. Collectively, our study demonstrates that p62 promotes Caspase 8 activation through autophagy flux blockage with cisplatin treatment. We have provided evidence that autophagy induction followed by its blockade increases cell sensitivity to chemotherapy which is dependent on p62-Caspase 8 mediated apoptosis signalling. p62 exhibits pro-death functions through its interaction with Caspase 8. p62 and Caspase 8 may become novel prognostic biomarkers and oncotargets for ovarian cancer treatment.

Genome sequencing analysis of a novel thermophilic strain Geobacillus sp. CX412.

The thermophilic spore-forming strain Geobacillus sp. CX412 was isolated from hot spring soil in Tengchong City, Yunnan Province, China. We sequenced the complete genome of Geobacillus sp. CX412 using PacBio SMRT Sequencing. Genome-scale phylogenetic analysis and average nucleotide identity (ANI) results indicated that Geobacillus sp. CX412 is a novel species in the genus Geobacillus. The metabolic potential of Geobacillus sp. CX412 based on COG, KEGG, and CAZymes analysis demonstrated that Geobacillus sp. CX412 was a highly adaptable strain with an unusually high number of 73 annotated transposons in the genome, which is relatively rare in Geobacillus. Compared with the near-derived strains, it was found that Geobacillus sp. CX412 has the unique ß-lactam resistance and more active metabolism (more than 50.5-100.1%). Additionally, its genome encodes glycoside hydrolases and other genes related to lignocellulose breakdown, suggesting that Geobacillus sp. CX412 has a considerable biomass degradation potential. Thus, Geobacillus sp. CX412 is a new thermophilic bacterial species that add to the increasing repertoire of known lignocellulose degraders.

The LINC00365/SCGB2A1 (Mammaglobin B) Axis Down-Regulates NF-κB Signaling and Is Associated with the Progression of Gastric Cancer.

PURPOSE: A lack of early diagnostic biomarkers and therapeutic targets has led to poor prognosis for gastric cancer patients. However, the analysis of cancer-associated genomic data has been shown to be effective in identifying potential markers. Recently, the long non-coding RNA LINC00365 and SCGB2A1 gene (as known as mammaglobin B) were predicted to be co-expressed in gastric cancer based on the Gene Expression Omnibus database. However, their precise role in gastric cancer tumors is still not clear. METHODS: The expressions of LINC00365 and SCGB2A1 in gastric cancer tissues were investigated using qPCR and their expressions were detected in a gastric cancer tissue microarray by in situ hybridization and immunohistochemical staining. The functions of LINC00365 in BGC-823 and MGC-803 gastric cancer cells were tested using the MTT assay, flow cytometry, colony formation assay, EDU staining, immunofluorescence and luciferase assay. RESULTS: We found that LINC00365 and SCGB2A1 mRNA were both expressed at low levels in 30 cases of gastric cancer. Gastric cancer tissue microarray analysis indicated that LINC00365 and SCGB2A1 were expressed at low levels in tumor tissue, and low expression of both factors correlated with shorter survival time. Functional studies showed that LINC00365 overexpression significantly inhibited gastric cancer cell viability through the impairment of proliferation rather than the promotion of apoptosis. Furthermore, overexpressed LINC00365 upregulated SCGB2A1 in gastric cancer cell lines. Immuno-fluorescence and luciferase assay analysis indicated that LINC00365 overexpression inhibited the NF-κB pro-survival signaling pathway. Consistent with the effects of LINC00365, SCGB2A1 upregulation also reduced cell survival and inactivated NF-κB. CONCLUSION: Collectively, our findings revealed that SCGB2A1 may be the target coding protein regulated by LINC00365 in gastric cancer. LINC00365 and SCGB2A1 may function as tumor suppressors and may serve as potential prognostic and therapeutic markers in gastric cancer treatment.

LINC00365-SCGB2A1 axis inhibits the viability of breast cancer through targeting NF-κB signaling.

Breast cancer is the most common high-grade malignancy in women. The lack of therapeutic targets has limited the treatment of breast cancer. Recently, long noncoding RNAs (lncRNAs) have been demonstrated to be dysregulated in various types of cancer. However, the specific mechanisms by which lncRNAs influence breast cancer have remained largely unclear. To bridge this research gap, the present study focused on the lncRNA LINC00365, which is expressed at a low level in breast cancer. Secretoglobin family 2A member 1 (SCGB2A1) was identified as a potential target protein regulated by LINC00365. The results of the present study demonstrated that the overexpression of LINC00365 and SCGB2A1 inhibited cell viability and induced cell apoptosis through the inhibition of the NF-κB signaling pathway in breast cancer cells. These findings indicated that LINC00365 may serve a crucial role in breast cancer and may be considered as a novel target for the clinical treatment of breast cancer.