Non-small cell lung cancer (NSCLC) remains a leading cause of mortality in the clinic. Previous studies have demonstrated that the NF-kappa-B activating protein like (NKAPL) is positively correlated with prognosis in several types of cancers. However, the role of NKAPL in the progression of NSCLC remains unclear. The expression and promoter methylation of NKAPL were examined by real-time PCR, quantitative PCR, and methylation-specific PCR. The functional impacts of NKAPL on NSCLC proliferation were explored by CCK8 assay and colony formation assay. Transwell assay was conducted to investigate the role of NKAPL in NSCLC cell migration and invasion, and the influence on metastasis was verified in vivo. Flow cytometry was exploited to analyze the influence on the cell cycle and apoptosis. The regulatory mechanism of NKAPL was investigated by immunoprecipitation-mass spectrometry, western blotting, immunofluorescence, and immunohistochemistry. NKAPL was down-regulated due to promoter methylation, which was associated with poor prognosis in NSCLC patients, while the up-regulation of NKAPL suppressed NSCLC cell proliferation and metastasis both in vitro and in vivo. Mechanistically, the NF-κB signaling pathway was inhibited because the up-regulation of NKAPL increased the stability and expression of TRIM21. NKAPL suppressed NSCLC cell proliferation and metastasis both in vitro and in vivo by increasing the stability and expression of TRIM21 and subsequently inhibiting the NF-κB signaling pathway.

Hepatic ischemia-reperfusion injury is an unavoidable surgical complication of liver transplantation and the leading cause of poor graft function and increased mortality post-transplantation. Multiple mechanisms have been implicated in ischemia-reperfusion injury; however, the characteristic changes at the transcriptional and metabolic levels in the early, intermediate, and late phases of ischemia-reperfusion injury remain unclear. In the study, mice underwent laparotomy following anesthesia, and the blood vessels of the liver were clipped using a vascular clamp to form 70% warm ischemia of the liver. Mouse liver sections and serum samples were collected and divided into the Sham, I1R12, I1R24, and I1R48 groups. Transcriptomics and metabolomics analyses were performed to study characteristic alterations during the early, intermediate, and late phases of ischemia-reperfusion injury. Quantitative real-time PCR was used to validate the critical differentially expressed genes. The differentially expressed genes and metabolites were identified by transcriptomics and metabolomics analyses. Moreover, GO and KEGG enrichment analyses indicated that glucose metabolism remodeling, inflammatory response activation, and lipid metabolism remodeling were characteristic changes in the early, intermediate, and late phases of ischemia-reperfusion injury, respectively. In summary, our study revealed the importance of glucolipid metabolism in ischemia-reperfusion injury and provided potential therapeutic intervention targets and a new perspective to explore the underlying mechanisms of ischemia-reperfusion injury.