Background The immunological checkpoint known as Inducible T Cell Costimulatory Factor (ICOS, Cluster of Differentiation, CD278) is activated and expressed on T cells. Both somatic cells and antigen-presenting cells expressed its ligand, ICOSL (including tumor cells in the tumor microenvironment).It is important for immunosuppression. Uncertainty surrounds the function of ICOS in tumor immunity. Methods Several bioinformatics techniques were employed by us to thoroughly examine the expression and prognostic value of ICOS in 33 cancers based on data collected from TCGA and GTEx. In addition, ICOS was explored with pathological stage, tumor-infiltrating cells, immune checkpoint genes, mismatch repair (MMR) genes, DNA methyltransferases (DNMTs), microsatellite instability (MSI),and tumor mutation burden (TMB).In addition,To ascertain the level of ICOS expression in various cells, qRT-PCR was employed. Results The findings revealed that ICOS expression was up regulation in most cancer types. The high expression of ICOS in tumor samples was related to the poor prognosis of UVM and LGG; The positive prognosis was boosted by the strong expression of ICOS in OV, SARC, SKCM, THYM, UCEC, and HNSC. The result is that the expression of malignancy was revealed by the immune cells’ invasion.profile of ICOS in different types of cancer. Different ways that ICOS expression is connected to immune cell infiltration account for variations in patient survival. Additionally, the TMB, MSI, MMR, and DNMT genes as well as ICOS expression are linked in many cancer types.The results of PCR showed that it is highly expressed in gastric, breast, liver and renal cell carcinoma cell lines compared with normal cells. Conclusion This study suggests that ICOS may be a potential tumor immunotherapy target and prognostic marker.
Background Brest cancer (BC) is the most common cancer in women and the second most frequent type of newly diagnosed cancer worldwide. Second, anoikis, a specific programmed death brought on by a cell's lack of contact with the extracellular matrix, is crucial for the spread of cancer. The impact of anoikis on BC patients' prognoses, however, is still unknown. Method Via the TCGA and GEO databases, we gathered patient transcriptome and clinical group data for this investigation. The classification of subtypes A and B, subtype survival analysis, and pathway analysis were performed using anoikis-related genes (ARGs). the least absolute shrinkage and selection operator (LASSO), multivariate Cox regression analysis, and tumor microenvironment were used to evaluate the immune microenvironment (TME). Ultimately, ten ARGs relevant to prognosis were collected, and prognostic models were created. In order to characterize the correlation of ARGS, we also performed single cell data analysis. Finally, we used real-time polymerase chain reaction (RT-PCR) to analyze the associations between the 10 prognostic ARGS and BC cells. Results By using Kaplan-Meier (KM) and receiver operating characteristic (ROC) curve analyses, we were able to identify ten ARGS (YAP1, PIK3R1, BAK1, PHLDA2, EDA2R, LAMB3, CD24, SLC2A1, CDC25C, and SLC39A6) as BC prognosis-related ARGS. These characteristics of the high-risk group of ARGS were linked to a poor prognosis in BC patients. KEGG functional analysis revealed that the immunological state of these high- and low-risk groups was different. By building a carcinogenesis model of risk score, risk score was found to be an independent prognostic factor. YAP1, PIK3R1, BAK1, PHLDA2, EDA2R, CD24, SLC2A1, and CDC25C were all strongly expressed in BC cells, according to the results of the RT-PCR analysis. were poorly expressed in SLC39A6 and LAMB3BC cells, but were strongly expressed in BC cells. The outcomes agreed with our earlier analysis of differential expression. Conclusion ARGS markers can be used as BC biomarkers for risk stratification and survival prediction in BC patients. Besides, ARGs can be used as stratification factors for individualized and precise treatment of BC patients.
Lactate was once considered to be a by‐product of energy metabolism, but its unique biological value was only gradually explored with the advent of the Warburg effect. As an end product of glycolysis, lactate can act as a substrate for energy metabolism, a signal transduction molecule, a regulator of the tumor microenvironment and immune cells, and a regulator of the deubiquitination of specific enzymes, and is involved in various biological aspects of tumor regulation, including energy shuttling, growth and invasion, angiogenesis and immune escape. Furthermore, we describe a novel lactate‐dependent epigenetic modification, namely histone lactylation modification, and review the progress of its study in tumors, mainly involving the reprogramming of tumor phenotypes, regulation of related gene expression, mediation of the glycolytic process in tumor stem cells (CSCs) and influence on the tumor immune microenvironment. The study of epigenetic regulation of tumor genes by histone modification is still in its infancy, and we expect that by summarizing the effects of lactate and histone modification on tumor and related gene regulation, we will clarify the scientific significance of future histone modification studies and the problems to be solved, and open up new fields for targeted tumor therapy.
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