Degradation of antibiotics by electrochemical advanced oxidation processes (EAOPs): Performance, mechanisms, and perspectives.

Global consumption and discharge of antibiotics have led to the rapid development and spread of bacterial antibiotic resistance. Among treatment strategies, electrochemical advanced oxidation processes (EAOPs) are gaining popularity for treating water/wastewater containing antibiotics due to their high efficiency and easiness of operation. In this review, we summarize various forms of EAOPs that contribute to antibiotic degradation, including common electrochemical oxidation (EO), electrolyte enhanced EO, electro-Fenton (EF) processes, EF-like process, and EAOPs coupling with other processes. Then we assess the performance of various EAOPs in antibiotic degradation and discuss the influence of key factors, including electrode, initial concentration and type of antibiotic, operation conditions, electrolyte, and water quality. We also review mechanisms and degradation pathways of various antibiotics degradation by EAOPs, and address the species and toxicity of intermediates produced during antibiotics treatment. Finally, we highlight challenges and critical research needs to facilitate the application of EAOPs in antibiotic treatment.

Comprehensive assessment of cellular senescence in the tumor microenvironment.

Cellular senescence (CS), a state of permanent growth arrest, is intertwined with tumorigenesis. Due to the absence of specific markers, characterizing senescence levels and senescence-related phenotypes across cancer types remain unexplored. Here, we defined computational metrics of senescence levels as CS scores to delineate CS landscape across 33 cancer types and 29 normal tissues and explored CS-associated phenotypes by integrating multiplatform data from ~20 000 patients and ~212 000 single-cell profiles. CS scores showed cancer type-specific associations with genomic and immune characteristics and significantly predicted immunotherapy responses and patient prognosis in multiple cancers. Single-cell CS quantification revealed intra-tumor heterogeneity and activated immune microenvironment in senescent prostate cancer. Using machine learning algorithms, we identified three CS genes as potential prognostic predictors in prostate cancer and verified them by immunohistochemical assays in 72 patients. Our study provides a comprehensive framework for evaluating senescence levels and clinical relevance, gaining insights into CS roles in cancer- and senescence-related biomarker discovery.

YY1 directly suppresses MYCT1 leading to laryngeal tumorigenesis and progress.

YY1 is a key transcription factor and plays different roles in various cancers. However, role and mechanism of YY1 in laryngeal cancer are still unknown. YY1 and MYCT1 mRNA and protein levels were detected by Real-time RT-PCR and Western Blot methods, respectively. Binding of YY1 to MYCT1 promoter was predicted and confirmed by bioinformatics and chromatin immunoprecipitation assays, respectively. MYCT1 promoter activity was assessed by dual luciferase assay system. Laryngeal cancer cell proliferation, migration, and apoptosis were evaluated by cell viability, colony formation, cell scratch assay, transwell assay, and flow cytometry methods, respectively. YY1 and MYCT1 were upregulated and downregulated at transcriptional level in laryngeal cancer, respectively, which showed a negative correlation between YY1 and MYCT1 expression in laryngeal cancer. Significantly higher expression of YY1 and lower expression of MYCT1 were found in laryngeal cancer tissues of patients with lymphatic metastasis than those without metastasis.YY1 directly bound to MYCT1 promoter region and inhibited its promoter activity. YY1 silence had similar biological functions as MYCT1 overexpression in repressiveness of proliferation and migration, and promotion of apoptosis in laryngeal cancer cells. However, the effects of YY1 silence were recovered by MYCT1 knockdown. YY1 promotes proliferation and migration with suppression of apoptosis via directly inhibiting MYCT1 in laryngeal cancer cells, suggesting that YY1 is a useful target as a potential oncogene in laryngeal cancer development and progression.