Aging is the deterioration of physiological mechanisms that is associated with getting old. There is a link between aging and mitochondrial function. However, there is an unresolved relationship between ATP levels and aging. To address this issue, we administered febuxostat (FBX), an inhibitor of human xanthine oxidase (XO)/xanthine dehydrogenase (XDH), to C. elegans. We used C. elegans as a model to evaluate the effects of FBX and to challenge the enigma of the relationship between ATP and lifespan. In this study, we showed that FBX protects mitochondria and prevents age-related muscle deterioration in C. elegans. In addition, we showed that FBX administration could increase ATP levels without overloading the mitochondria while extending the lifespan. We also showed that the combination of FBX and an antioxidant as a protection against ROS prolongs lifespan more. We have shown that the antioxidant effects and increased ATP levels may lead to antiaging effects.

Cancer is one of the main causes of human death. Here, we focus on the B-cell lymphoma 7 protein family member B (BCL7B) gene, an accessory subunit of the SWI/SNF chromatin-remodelling complex. To characterize the function of BCL7B, heterozygous BCL7B-deficient stomach cancer cell lines were generated with the CRISPR/Cas9 genome editing system. The comprehensive gene expression patterns were compared between parental cells and each ΔBCL7B cell line by RNA-seq. The results showed marked downregulation of immune-related genes and upregulation of stemness-related genes in the ΔBCL7B cell lines. Moreover, by ChIP-seq analysis with H3K27me3 antibody, the changes of epigenetic modification sequences were compared between parental cells and each ΔBCL7B cell line. After machine learning, we detected the centroid sequence changes, which exerted an impact on antigen presentation. The regulation of BCL7B expression in cancer cells gives rise to cancer stem cell-like characteristics and the acquisition of an immune evasion phenotype.

Aging is the deterioration of physiological mechanisms that is associated with getting old. There is a link between aging and mitochondrial function. In C. elegans, it has been reported that inhibiting the electron transfer system decreases ATP production and extends lifespan. However, it has also been suggested that energy loss due to mitochondrial dysfunction or impairment is a mechanism of diseases and aging. Thus, there is an unresolved relationship between ATP levels and aging. To address this issue, we administered febuxostat (FBX), an inhibitor of human xanthine oxidase (XO)/xanthine dehydrogenase (XDH), to C. elegans. XO/XDH is an enzyme that participates in the in vivo synthesis of uric acid. When FBX is added to cells, the salvage pathway of purine metabolism becomes dominant, and the ATP concentration increases. Since humans and C. elegans but few mammalian species lack uricase, which degrades uric acid, we used C. elegans as a model to evaluate the effects of FBX and to challenge the enigma of the relationship between ATP and lifespan.In this study, we showed that FBX protects mitochondria and prevents age-related muscle deterioration in C. elegans. In addition, we showed that FBX administration could increase ATP levels without overloading the mitochondria while extending the lifespan. We also showed that the combination of FBX and an antioxidant as a protection against ROS prolongs lifespan more. We have shown that the antioxidant effects and increased ATP levels may lead to antiaging effects.