PurposeTo unravel the oncogenic role of CDCA4 in different cancers from the perspective of tumor immunity.MethodsRaw data on CDCA4 expression in tumor samples and paracancerous samples were obtained from TCGA and GTEX databases. In addition, we investigated pathological stages and the survival analysis of CDCA4 in pan-cancer across Gene Expression Profiling Interactive Analysis (GEPIA) database. Cox Proportional Hazards Model shows that high CDCA4 levels are associated with several vital indicators in oncology. On the one hand, we explored the correlation between CADA4 expression and tumor immune infiltration by the TIMER tool; On the other hand, we utilized the methods of CIBERSORT and ESTIMATE computational to evaluate the proportion of tumor infiltrating immune cells (TIIC) and the amounts of stromal and immune components based on TCGA database. The use of antineoplastic drugs and the expression of CDCA4 also showed a high correlation via linear regression. Protein–Protein Interaction analysis was performed in the GeneMANIA database, and enrichment analysis was performed and predicted signaling pathways were identified by using Gene Ontology and Kyoto Encyclopedia of Genes. The correlation between CDCA4 expression with Copy number variations (CNV) and methylation is detailed, respectively. Molecular biology experiments including Western blotting, flow cytometry, EDU staining, Transwell and Wound Healing assay to validate the cancer promoting role of CDCA4 in hepatocellular carcinoma (HCC).ResultsMost tumors highly expressed CDCA4. Elevated CDCA4 expression was associated with poor OS and DFS. There was a significant correlation between CDCA4 expression and TITCs. Moreover, markers of TIICs exhibited distinct patterns of CDCA4 associated immune infiltration. In addition, we pay attention to the association between the expression of CDCA4 and the use of the anti-tumor drugs. CDCA4 is related to biological progress (BP), cellular component (CC) and molecular function (MF). Dopaminergic Synapse, AMPK, Sphingolipid, Chagas Disease, mRNA Surveillance were significantly enriched pathways in positive and negative correlation genes with CDCA4. CNV is thought to be a positive correlation with CDCA4 expression. Conversely, methylation is negative correlation with CDCA4 expression. Molecular biology experiments confirm a cancer promoting role for CDCA4 in HCCConclusionCDCA4 may serve as a biomarker for cancer immunologic infiltration and poor prognosis, providing a new way of thinking for cancer treatment.

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infects both people and animals and may cause significant respiratory problems, including lung illness: Corona Virus Disease 2019 (COVID-19). Swabs taken from the throat and nose of people who have the illness or are suspected of having it have shown this pathogenic virus. When SARS-CoV-2 infects the upper and lower respiratory tracts, it may induce moderate to severe respiratory symptoms, as well as the release of pro-inflammatory cytokines including interleukin 6 (IL-6). COVID-19-induced reduction of IL-6 in an inflammatory state may have a hitherto undiscovered therapeutic impact. Many inflammatory disorders, including viral infections, has been found to be regulated by IL-6. In individuals with COVID-19, one of the primary inflammatory agents that causes inflammatory storm is IL-6. It promotes the inflammatory response of virus infection, including the virus infection caused by SARS-CoV-2, and provides a new diagnostic and therapeutic strategy. In this review article, we highlighted the functions of IL-6 in the coronavirus, especially in COVID-19, showing that IL-6 activation plays an important function in the progression of coronavirus and is a rational therapeutic goal for inflammation aimed at coronavirus.

It is worth noting that neuroinflammation is well recognized as a symptom of neurodegenerative diseases (NDs). The regulation of neuroinflammation becomes an attractive focus for innovative ND treatment technologies. There is evidence that IL-22 is associated with the development and progression of a wide assortment of NDs. For example, IL-22 can activate glial cells, causing them to generate pro-inflammatory cytokines and encourage lymphocyte infiltration in the brain. IL-22 mRNA is highly expressed in Alzheimer’s disease (AD) patients, and a high expression of IL-22 has also been detected in the brains of patients with other NDs. We examine the role of IL-22 in the development and treatment of NDs in this review, and we believe that IL-22 has therapeutic potential in these diseases.

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Background: Head and neck squamous cell carcinoma (HNSCC) is a highly prevalent and malignant tumor that is difficult to effectively prognosticate outcomes. Recent reports have suggested that inflammation is strongly related to tumor progression, and several biomarkers linked to inflammation have been demonstrated to be useful for making a prognosis. The goal of this research was to explore the relevance between the inflammatory-related genes and HNSCC prognosis.Methods: The clinical information and gene expression data of patients with HNSCC were acquired from publicly available data sources. A multigene prognostic signature model was constructed in The Cancer Genome Atlas and verified in the Gene Expression Omnibus database. According to the risk score calculated for each patient, they were divided into low- and high-risk groups based on the median. The Kaplan–Meier survival curve and receiver operating characteristic curve were applied to determine the prognostic value of the risk model. Further analysis identified the independent prognostic factors, and a prognostic nomogram was built. The relationship between tumor immune infiltration status and risk scores was investigated using Spearman correlation analysis. Finally, to confirm the expression of genes in HNSCC, quantitative real-time polymerase chain reaction (qRT-PCR) was performed.Results: A prognostic model consisting of 14 inflammatory-related genes was constructed. The samples with a high risk had an apparently shorter overall survival than those with a low risk. Independent prognostic analysis found that risk scores were a separate prognostic factor in HNSCC patients. Immune infiltration analysis suggested that the abundance of B cells, CD8 T cells, M2 macrophages, myeloid dendritic cells, and monocytes in the low-risk group was higher, while that of M0, M1 macrophages, and resting NK cells was obviously higher in the high-risk group. The risk scores were related to chemotherapeutic sensitivity and the expression of several immune checkpoint genes. Moreover, CCL22 and IL10 were significantly higher in HNSCC tissues, as determined by qRT-PCR.Conclusion: Taken together, we constructed a novel inflammatory response–related gene signature, which may be used to estimate outcomes for patients with HNSCC and may be developed into a powerful tool for forecasting the efficacy of immunotherapeutic and chemotherapeutic drugs for HNSCC.