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An abnormality in the regulation of adenosine deaminase acting on RNA (ADAR) enzymes, which catalyzed adenosine-to-inosine (A-to-I) RNA editing, was closely associated with the highly aggressive biologic behavior and poor prognosis in many malignancies. In the present study, we aimed to investigate the relationship among transcript factors-microRNAs regulatory network, immune environment, and ADAR gene in colorectal carcinoma (CRC). The association among the expression levels of ADAR mRNA and copy number variation, methylation, and mutation status were comprehensively analyzed using cBioPortal, Wanderer, and UALCAN databases in CRC datasets. ADAR-transcript factors (TFs) and ADAR-miRNA regulation networks were constructed by Cistrome Cancer and miRWalk2.0, respectively. The full network and subnetworks for ADAR coexpression genes were constructed using the STRING database and visualized by the MCODE module of the Cytoscape app. The relationship between ADAR mRNA expression and the abundance of infiltrating immune cells in CRC patients was explored by the Tumor Immune Estimation Resource, CIBERSORT, and single-gene gene set enrichment analysis (GSEA). ADAR mRNA was elevated and was a cancer essential gene in CRC. ADAR mRNA and transcripts P110 were significantly elevated in CRC compared to normal controls. Low-level methylation in the promoter region and high copy number amplification of ADAR were responsible for high levels of ADAR mRNA expression. ADAR coexpression genes were mainly involved in immunoregulation, especially T-lymphocyte activation. Hub genes, including CD2, CD274, and FASLG, were also significantly upregulated in the ADAR-high group compared to the control group. Besides, M1 macrophages were enriched in the ADAR-high group compared to the control group. This study demonstrated that ADAR, a new essential gene, was involved in the immune regulator and was a novel immune treatment target in CRC. [ABSTRACT FROM AUTHOR]

PubMed, ScienceDirect, Cochrane, Embase, Scopus, China National Knowledge Infrastructure (CNKI), Chinese Weipu, and Wanfang databases were searched to evaluate the effects of probiotics supplements on gastric cancer‐related inflammatory factors. Parallel randomized controlled trials (RCTs) assessing the effects of prebiotics supplement on gastric cancer patients were included in the review. Compared with routine nutrition, meta‐analysis shows that probiotics supplements reduce gastric cancer‐related inflammation levels by mostly increasing the levels of cluster of differentiation 4+ and greatly reducing the levels of interleukin‐6. Probiotics supplements can control the inflammatory response in cancer patients and may be a potential approach for controlling inflammatory levels in the patients. However, a larger population is needed for further study because of a certain degree of heterogeneity in this review. Practical applications: The effects of probiotics (Bifidobacterium, Lactobacillus, and Streptococcus species) on the gastric cancer‐related inflammation were investigated.Probiotics can reduce gastric cancer‐related inflammation levels more effectively by increasing the levels of cluster of differentiation 4+ and greatly reducing the levels of interleukin‐6.The study provides some theoretical basis for controlling cancer‐related inflammation responses in the patients using probiotics. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) is a common tumor-associated lethal disease, and invasiveness and metastasis are primary challenges in its clinical treatment. Hypoxia microenvironment cannot be ignored in the process of metastasis. Hypoxia inducible factor-1α (HIF-1α) is the core component of the hypoxia signaling pathway. The aim of this study was to identify potential hub genes and signaling pathways associated with HIF-1α. We explored the invasiveness- and metastasis-associated phenotype of GC via bioinformatics analysis and molecular studies. Differentially expressed genes (DEGs) were identified in GC cells and HIF-1α-knockdown GC cells. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed, and a protein-protein interaction (PPI) network was constructed. Hub genes were identified via centrality analysis and Molecular Complex Detection (MCODE) module analysis. The findings suggested that prolyl 4-hydroxylase beta polypeptide (P4HB) has strong associations with HIF-1α. Further, we observed that HIF-1α and P4HB were upregulated in SGC-7901 and BGC-823 cells. In addition, inhibition of HIF-1α expression reduced invasion and metastasis in GC cells; this effect was partially reversed by P4HB overexpression. Our results confirm that P4HB plays a significant role in the regulatory network of HIF-1α. Therefore, HIF-1α and P4HB may be considered potential biomarkers of GC. [ABSTRACT FROM AUTHOR]