CD8⁺ T cells are an important component of the body’s adaptive immune response. During viral or intracellular bacterial infections, CD8⁺ T cells are rapidly activated and differentiated to exert their immune function by producing cytokines. Alterations in the glycolysis of CD8⁺ T cells have an important effect on their activation and function, while glycolysis is important for CD8⁺ T cell functional failure and recovery. This paper summarizes the importance of CD8⁺ T cell glycolysis in the immune system. We discuss the link between glycolysis and CD8⁺ T cell activation, differentiation, and proliferation, and the effect of altered glycolysis on CD8⁺ T cell function. In addition, potential molecular targets to enhance and restore the immune function of CD8⁺ T cells by affecting glycolysis and the link between glycolysis and CD8⁺ T cell senescence are summarized. This review provides new insights into the relationship between glycolysis and CD8⁺ T cell function, and proposes novel strategies for immunotherapy by targeting glycolysis.

Fibroblasts are highly heterogeneous mesenchymal stromal cells, and different fibroblast subpopulations play different roles. A subpopulation of fibroblasts expressing CD90, a 25–37 kDa glycosylphosphatidylinositol anchored protein, plays a dominant role in the fibrotic and pro-inflammatory state. In this review, we focused on CD90⁺ fibroblasts, and their roles and possible mechanisms in disease processes. First, the main biological functions of CD90⁺ fibroblasts in inducing angiogenesis and maintaining tissue homeostasis are described. Second, the role and possible mechanism of CD90⁺ fibroblasts in inducing pulmonary fibrosis, inflammatory arthritis, inflammatory skin diseases, and scar formation are introduced, and we discuss how CD90⁺ cancer-associated fibroblasts might serve as promising cancer biomarkers. Finally, we propose future research directions related to CD90⁺ fibroblasts. This review will provide a theoretical basis for the diagnosis and treatment CD90⁺ fibroblast-related disease.

Introduction: Gliomas, especially the glioblastomas, are one of the most aggressive intracranial tumors with poor prognosis. This might be explained by the heterogeneity of tumor cells and the inhibitory immunological microenvironment. Dendritic cells (DCs), as the most potent in vivo functional antigen‐presenting cells, link innate immunity with adaptive immunity. However, their function is suppressed in gliomas. Therefore, overcoming the dysfunction of DCs in the TME might be critical to treat gliomas.Method: In this paper we proposed the specificity of the glioma microenvironment, analyzed the pathways leading to the dysfunction of DCs in tumor microenvironment of patients with glioma, summarized influence of DC‐based immunotherapy on the tumor microenvironment and proposed new development directions and possible challenges of DC vaccines.Result: DC vaccines can improve the immunosuppressive microenvironment of glioma patients. It will bring good treatment prospects to patients. We also proposed new development directions and possible challenges of DC vaccines, thus providing an integrated understanding of efficacy on DC vaccines for glioma treatment.

Head and neck cancer (HNC) is mainly treated by surgery, radiotherapy, and adjuvant chemotherapy; however, the prognosis of some patients with HNC is poor because of radiotherapy and chemotherapy resistance. In recent years, anti‑PD‑1 monoclonal antibodies have shown certain efficacy, and a change of the tumor immune microenvironment is the main reason for the failure of HNC immunotherapy. The present study aimed to identify and verify that CD38, which is closely related to the prognosis of HNC, is a potential biological marker of radiotherapy and chemotherapy resistance and PD-L1 immunotherapy resistance via a comprehensive bioinformatic analysis in The Cancer Genome Atlas and Gene Expression Omnibus databases. According to the UALCAN database, the transcript level of CD38 in HNC was analyzed using cluster analysis, and the expression of CD38 mRNA in HNC was detected using the Oncomine database. The characteristics of CD38-related oncogenes were identified by gene cluster enrichment analysis in LinkedOmics. The R2 and SEER databases were used to further evaluate the prognostic significance of the CD38 gene in HNC using receiver operating characteristic curve analysis of Kaplan-Meier (KM) survival and the clinical characteristics of the subjects. The protein-protein interaction network of the top 50 genes showing significant positive correlations with CD38 in HNC was analyzed using STRING. Finally, we used a nasopharyngeal carcinoma (NPC) cell line to verify the biological function. The results showed that the levels of CD38 mRNA expression in patients with HNC were significantly higher than those in healthy controls. The levels of CD38 mRNA expression in patients with HNC of different ages, sexes, and races were significantly higher than those in the healthy controls. CD38 is an independent prognostic factor for HNC, and high expression of CD38 indicates poor prognosis. CD38 expression correlated positively with the markers of many kinds of immune cells, and correlated significantly with the expression of PD-L1. We found that the high expression of CD38 suggested a poor prognosis in the subgroup of tumors treated with chemotherapeutic drugs in the G1/S phase. We used HNC cell lines to verify that the high expression of CD38 promoted the proliferation of NPC cells and produced radiotherapy tolerance. Through comprehensive bioinformatics analysis, we suggested that CD38 is a key gene involved in radiotherapy, chemotherapy, and immune drug resistance in HNC. This study provides a reliable biomarker to predict the prognosis of patients with HNC and a reference for clinical comprehensive treatment of HNC. Individualization combined with CD38 monoclonal antibodies might provide a promising treatment strategy for this fatal disease, and this comprehensive treatment might reduce the damage to normal tissue and improve the prognosis and quality of life of patients with HNC.

YBX1 is a member of the Y-box transcription factor family and is a multifunctional RNA/DNA-binding protein characterized by a highly conserved cold shock domain (CSD). YBX1 is localized in both the cytoplasm and nucleus, where it participates in various biological processes such as transcription, translation, and DNA damage repair. YBX1 is upregulated in numerous malignant tumors and is closely associated with tumor progression and poor prognosis, making it a recognized target for cancer therapy. This review introduces the role and mechanism of YBX1 in tumor progression, its function in embryonic development, bone differentiation, cartilage formation, and adipogenesis, the impact of upstream regulatory factors on its function, as well as the relationship between YBX1 and disease prognosis and treatment outcomes. This review aims to provide a comprehensive perspective on the function of YBX1.

In contrast to normal cells, cancer cells typically undergo metabolic reprogramming. Studies have shown that oncogenes play an important role in this metabolic reprogramming. CD38 is a multifunctional transmembrane protein that is expressed abnormally in a variety of tumor types. To investigate the effect and possible mechanism of CD38 in cervical cancer cells and to provide a new therapeutic target for the treatment of cervical cancer, the present study identified that CD38 is involved in regulating cell metabolism in cervical cancer cells. Liquid chromatography-tandem mass spectrometry and bioinformatic analyses revealed that differentially abundant proteins in CD38-overexpressed cervical cancer cells (CaSki-CD38 and HeLa-CD38) are predominantly involved in glycolytic pathways, oxidative phosphorylation and the NAD/NADH metabolic process. Further experiments using an ATP test kit and lactate test kit revealed that CD38 promotes glucose consumption, increases lactate accumulation and increases ATP production. In addition, CD38 increases the phosphorylation of phosphatidylserine/threonine kinase (AKT), mechanistic target of rapamycin (mTOR) and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), which play a key role in tumor metabolism. Furthermore, it was found that the energy metabolism of cervical cancer cells was inhibited following treatment with the mTOR inhibitor rapamycin. In conclusion, the results of the present study suggested that CD38 regulates the metabolism of cervical cancer cells by regulating the PI3K/AKT/mTOR pathway, which may be a candidate target for the treatment of cervical cancer.