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Chimeric antigen receptor (CAR) T cell therapy is a promising cancer treatment modality. The breakthroughs in CAR T cell therapy were, in part, possible with the help of cell analysis methods, such as single‐cell analysis. Bulk analyses have provided invaluable information regarding the complex molecular dynamics of CAR T cells, but their results are an average of thousands of signals in CAR T or tumour cells. Since cancer is a heterogeneous disease where each minute detail of a subclone could change the outcome of the treatment, single‐cell analysis could prove to be a powerful instrument in deciphering the secrets of tumour microenvironment for cancer immunotherapy. With the recent studies in all aspects of adoptive cell therapy making use of single‐cell analysis, a comprehensive review of the recent preclinical and clinical findings in CAR T cell therapy was needed. Here, we categorized and summarized the key points of the studies in which single‐cell analysis provided insights into the genomics, epigenomics, transcriptomics and proteomics as well as their respective multi‐omics of CAR T cell therapy. [ABSTRACT FROM AUTHOR]

Cervical cancer is one of the most common cancers in women and is the third leading cause of cancer-related mortality. Metabolic dysregulation is a common hallmark of cancer. Reactive oxygen species (ROS) are oxygen metabolism byproducts that are impacted by metabolic instability. ROS can trigger cellular apoptosis as a safety switch by controlling the intrinsic mitochondrial apoptosis pathway. MSRB3(methionine sulfoxide reductase B3) can inhibit ROS-mediated apoptosis in cervical cancer cells, promoting tumorigenesis and metastasis. In this article, the effect of miR-331-3p, and miR-338-3p on reducing gene expression is investigated. The unfavorable proteins in cervical cancer tissues were selected and obtained using the Human Protein Atlas (HPA) database. OncoDB was used to find differentially expressed genes (DEGs) linked with the cancer stage. A Venn diagram was created to identify genes that are both clinically unfavorable and linked with the cancer stage. STRING database was used to predict functional interactions of human proteins with specific genes. The upstream transcription factor, Gene Ontology analysis, and potential mechanism of MSRB3 and its interacting proteins were all investigated using Enrichr. HPA identified 223 genes linked with poor prognosis in cervical cancer patients. OncoDB was used to identify the top 1,000 DEGs related to cervical cancer patients' clinical stages. MSRB3 expression was shown to be correlated with cervical cancer patient survival and clinical stage. A tight relationship between MSRB3 expression and ROS was discovered by Reactome. According to STRING, MSRB3 interacts with two additional genes (TXN(Thioredoxin) and FXN(Frataxin)). According to GO analysis, these genes were engaged in protein repair pathways and had oxidoreductase activity. We discovered that MSRB3 expression is associated with a poor prognosis and survival in cervical cancer patients. Using the miRWalk database, we predicted that the miR-331-3p, miR-338-3p, and hsa-let-7b-3p have the potential to be involved in regulating MSRB3 Also, due to the TRRUST analysis, HSF2 is an upstream transcription factor of MSRB3, TXN, and FXN can be knocked down in order to suppress MSRB3 with two additional genes. Thus, treatment strategies that target MSRB3 expression may prone cervical cancer cells to apoptosis. [ABSTRACT FROM AUTHOR]

Interleukin (IL)-33, a member of IL-1 cytokine family, is produced by various immune cells and acts as an alarm to alert the immune system after epithelial or endothelial cell damage during cell necrosis, infection, stress, and trauma. The biological functions of IL-33 largely depend on its ligation to the corresponding receptor, suppression of tumorigenicity 2 (ST2). The pathogenic roles of this cytokine have been implicated in several disorders, including allergic disease, cardiovascular disease, autoimmune disease, infectious disease, and cancers. However, alerted levels of IL-33 may result in either disease amelioration or progression. Genetic variations of IL33 gene may confer protective or susceptibility risk in the onset of autoimmune diseases. The purpose of this review is to discuss the involvement of IL-33 and ST2 in the pathogenesis of a variety of autoimmune disorders, such as autoimmune rheumatic, neurodegenerative, and endocrine diseases. [ABSTRACT FROM AUTHOR]