Background: Acute myeloid leukemia(AML) is a malignant clonal disease. As the most common type of leukaemia, it is characterised by poor treatment outcomes and a poor prognosis in both the paediatric and adult populations. Improving anti-tumour responses through immunomodulators is a promising strategy or a new avenue for AML treatment. Methods: Using publicly available data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx), we examined the association between SAM And SH3 Domain Containing 3(SASH3) and AML. Wilcoxon signed-rank test and logistic regression were used to analyze the relationship between clinical pathologic features and SASH3. Cox regression and Kaplan-Meier methods were used to determine the clinical characteristics associated with overall survival in patients with AML. Then the relationship between immune infiltration and SASH3 was also analyzed. The research finding was validated by data from the Gene Expression Omnibus (GEO) database. Results: Compared to normal patients, SASH3 expression in AML patients was significantly higher (p = 3.05e-34) and strongly associated with survival. In addition, SASH3 expression was significantly correlated with survival outcome (p = 5.3E-03) and cytogenetic risk (p = 3E-04) in AML. SASH3 expression was correlated with the expression of the genes HCK, SYK, FYN, ITGB2, PIK3CD, FGR, PIK3R5, VAV1, LCP2, and GRB2. Our study suggests that SASH3 expression is strongly associated with AML development and survival outcomes as well as multiple cancer-related genes and pathways, such as the HCK(Hematopoietic cell kinase) and regulation of small GTPase-mediated signal transduction. Conclusion: Our study revealed that SASH3 expression is closely associated with AML development and survival outcome, as well as multiple cancer-related genes and pathways, thus highlighting SASH3 as a potential therapeutic marker of AML.

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This study examined the prognostic role of CENPW in clear cell renal cell carcinoma (ccRCC) using publicly available data from The Cancer Genome Atlas (TCGA). In order to clarify the relationship between clinicopathological features and CENPW expression information obtained from the TCGA database, logistic regression analysis was applied. Moreover, the expression of CENPW was closely associated with multiple immune cell infiltrations, as determined by immune cell infiltration analysis. Kaplan-Meier survival analysis demonstrated that the lower the expression of CENPW, the better the prognosis (p < 0.001), indicating that CENPW is an important risk factor for patients with ccRCC. In addition, CENPW expression was also significantly associated with T stage (p < 0.001), N stage (p = 0.011), M stage (p = 0.001), Pathologic stage (p < 0.001) and Histologic stage (p < 0.001). It was found that CENPW could be an independent prognostic factor in both univariate and multivariate Cox regression analyses (p < 0.05). The results of GSEA analysis showed that CENPW was closely associated with several immune-related signaling pathways. Furthermore, in ccRCC, the expression of CENPW was closely associated with the infiltration of various immune cells and the expression of multiple immune cell gene markers. Finally, we verified the expression levels of CENPW using three different datasets from the Gene Expression Omnibus (GEO) database. The results of survival outcomes on GEPIA2 website were similar to the survival curves drawn based on TCGA database (all P < 0.05). In conclusion, we conclude that CENPW is a potential independent prognostic marker for ccRCC and plays an essential role in the tumor microenvironment by regulating immune cell infiltration.

Background: Dietary interventions are one of the most common health promotion tools. Regular intermittent fasting is thought to reduce body weight and ameliorate adverse cardiovascular disease factors significantly. However, there is growing evidence that fasting positively affects body composition and biochemical parameters, but very few studies related to its mechanisms. In this study, bioinformatics network analysis was performed to investigate the effects of fasting on adipose and muscle tissues and further explore the potential mechanisms and targets of action. Methods: We downloaded the adipose tissue and muscle tissue gene expression datasets before and after fasting from the Gene Expression Omnibus (GEO) database and constructed co-expression networks by Weighted correlation network analysis (WGCNA) to identify key modules. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed for the differential genes in adipose tissue and muscle tissue-related modules, respectively. Then, we constructed protein-protein interaction (PPI) networks using the STRING database and detected the central genes in the networks. Results: Functional enrichment analysis showed that AMPK pathway and neurodegenerative disease-related pathways might be involved in the regulation of fasting in humans. PPI network construction indicated that the regulation of fasting in humans, both in adipose and muscle tissues, may be associated with two central genes, TXNIP and DLAT, and that this regulation is likely to act on human metabolism. Conclusion: Our work indicates that a total of 15 key genes, including TXNIP, DLAT, PDK4, DDIT3, and PFKFB3, may receive regulation by fasting interventions, especially TXNIP and DLAT are the basis of fasting mechanisms in adipose and muscle tissues. The pathways regulated by these key genes may provide new targets for further studies on the mechanism of fasting and the treatment of metabolic diseases.