Identification of Key Biomarkers and Candidate Molecules in Non-Small-Cell Lung Cancer by Integrated Bioinformatics Analysis.

Background: Non-small cell lung cancer (NSCLC) is the most prevalent malignant tumor of the lung cancer, for which the molecular mechanisms remain unknown. In this study, we identified novel biomarkers associated with the pathogenesis of NSCLC aiming to provide new diagnostic and therapeutic approaches for NSCLC by bioinformatics analysis. Methods: From the Gene Expression Omnibus database, GSE118370 and GSE10072 microarray datasets were obtained. Identifying the differentially expressed genes (DEGs) between lung adenocarcinoma and normal samples was done. By using bioinformatics tools, a protein-protein interaction (PPI) network was constructed, modules were analyzed, and enrichment analyses were performed. The expression and prognostic values of 14 hub genes were validated by the GEPIA database, and the correlation between hub genes and survival in lung adenocarcinoma was assessed by UALCAN, cBioPortal, String and Cytoscape, and Timer tools. Results: We found three genes (PIK3R1, SPP1, and PECAM1) that have a clear correlation with OS in the lung adenocarcinoma patient. It has been found that lung adenocarcinoma exhibits high expression of SPP1 and that this has been associated with poor prognosis, while low expression of PECAM1 and PIK3R1 is associated with poor prognosis (P < 0.05). We also found that the expression of SPP1 was associated with miR-146a-5p, while the high expression of miR-146a-5p was related to good prognosis (P < 0.05). On the contrary, the lower miR-21-5p on upstream of PIK3R1 is associated with a higher surviving rate in cancer patients (P < 0.05). Finally, we found that the immune checkpoint genes CD274(PD-L1) and PDCD1LG2(PD-1) were also related to SPP1 in lung adenocarcinoma. Conclusions: The results indicated that SPP1 is a cancer promoter (oncogene), while PECAM1 and PIK3R1 are cancer suppressor genes. These genes take part in the regulation of biological activities in lung adenocarcinoma, which provides a basis for improving detection and immunotherapeutic targets for lung adenocarcinoma.

Children and Urban Green Infrastructure in the Digital Age: A Systematic Literature Review.

In the digital age, time spent outdoor in green areas is significantly decreasing for children living in cities. With the advent of digital technology, a series of digital tools are gradually integrated into children's lives and act as a double-edged sword: on the one hand, an increasing number of children tend to stay at home and play digital games instead of interacting with nature; on the other hand, new digital technology is increasingly being used to engage children with outdoor activities. A host of studies have investigated children's behaviour in the natural environment. However, a systematic literature review of children's interaction with the urban green infrastructure (UGI) and the respective role of digital environment, based on a theoretical framework that explicitly takes the multi-level determinants and individual-level mechanism of behaviour change into account does not exist yet. This work provides a conceptual framework that covers various determinants, such as motivation, capability, and opportunity related factors of children's behaviour in terms of their UGI interaction at the city and neighbourhood levels, while taking into account the individual-level mechanism of behavioural change and the role of the digital environment. The framework is used to systematically review recent international empirical evidence on the determinants of children-UGI interaction. The results are useful for laying the theoretical foundation for future empirical research on children-UGI interaction, specifically in the presence of digital interventions. They also provide urban/digital intervention designers and policymakers with theory-based design and policy guidelines for the creation of child-friendly UGI.

Activation of Aurora A kinase increases YAP stability via blockage of autophagy.

Transcription cofactor Yes-associated protein (YAP) plays an important role in cancer progression. Here, we found that Aurora A kinase expression was positively correlated with YAP in lung cancer. Aurora A depletion suppresses lung cancer cell colony formation, which could be reversed by YAP ectopic overexpression. In addition, activation of Aurora A increases YAP protein abundance through maintaining its protein stability. Consistently, the transcriptional activity of YAP is increased upon Aurora A activation. We further showed that shAURKA suppressed YAP expression in the absence of Lats1/2, indicating that Aurora A regulates YAP independently of Hippo pathway. Instead, Aurora A induced blockage of autophagy to up-regulate YAP expression. Collectively, our findings provide insights into regulatory mechanisms of YAP expression in lung cancer development.