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Ferroptosis is a type of regulated cell death (RCD), and it plays an important role in the occurrence of diseases, especially the development of tumors. Ferroptosis of tumor cells affects the antitumor immunity and the immune response to treatment to varying degrees. Ferroptosis also plays a key role in immune cells. This review outlines the mechanism of the immune-related effects of ferroptosis pathways in tumor progression and treatment, and it discusses potential methods for improving antitumor immunity and enhancing the efficacy of current cancer treatments by targeting ferroptosis.

Leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1), is an immunosuppressive receptor, widely expressed by immune cells, but the part of LAIR-1 in glioma progression remains unclear. The purpose of this study was to explore the relationship between LAIR-1 expression and the development of lower-grade glioma (LGG) using publicly available data sets.We took advantage of The Cancer Genome Atlas (TCGA) to analyze the expression of LAIR-1 in patients with LGG. Second, Kaplan-Meier methods and univariate and multivariate Cox regression analyses were used to examine the clinical significance of LAIR-1 expression in combination with CGGA databases, and then receiver operating characteristic curve analysis was used to verify the prognostic utility of LAIR-1. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene set enrichment analysis (GSEA) were used to explore the function of LAIR-1. Analysis of the correlation with immune infiltration was conducted using the ESTIMATE algorithm and single sample gene set enrichment analysis.Our results showed that LAIR-1 expression to be positively correlated with malignant clinicopathologic features of LGG. Univariate analysis and multivariate analysis revealed that overexpression of LAIR-1 was correlated with a worse prognosis in patients. A nomogram model combining LAIR-1 was more useful in guiding clinical diagnosis, and functional enrichment analysis showed that malignant development of glioma was closely affiliated with the tumor immune microenvironment.These results indicate that LAIR 1 is a latent marker for determining the prognosis of LGG patients. LAIR 1 may also participate a critical part in TIME of LGG by regulating the infiltration of immune cells, suggesting that LAIR 1 might be used as a therapeutic target to regulate the antitumor immune response.

The therapeutic effects of conventional treatment on gliomas are not promising. The tumor microenvironment (TME) has a close association with the invasiveness of multiple types of tumors, including low-grade gliomas (LGG). This study aims to validate the prognostic and immune-related role of macrophage scavenger receptor 1 (MSR1) in LGG patients.Data in this study were obtained from public databases. The differential expression of MSR1 was analyzed in LGG patients with different clinicopathological characteristics. Kaplan-Meier survival analysis, a time-dependent receiver operating characteristic (ROC) curve, and Cox regression analysis were used to assess the prognostic value of MSR1. Differentially expressed genes (DEGs) were screened between the high and low expression groups of MSR1. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to annotate the function of these DEGs. Hallmark gene sets were identified based on MSR1 by Gene Set Enrichment Analysis (GSEA). Difference analysis and correlation analysis were used to study the relationship between MSR1 and TME-related scores, tumor-infiltrating immune cells (TIICs), immune-related gene sets, and immune checkpoints (ICPs). The single-cell sequencing data were processed to identify the cell types expressing MSR1. The quantification of TIICs in TME was calculated by single-sample gene set enrichment analysis (ssGSEA). The differential expression of MSR1 in LGG and control brain tissues was verified by experiments.There were significant differences in the expression level of MSR1 in different types of tissues and cells. MSR1 has a high prognostic value in LGG patients and can be used as an independent prognostic factor. MSR1 is closely related to TME and may play an important role in the immunotherapy of LGG patients.The result of our study demonstrated that MSR1 is an independent prognostic biomarker in LGG patients and may play an important role in the TME of LGGs.

Increasing evidence from structural and functional studies has indicated that protein disulphide isomerase (PDI) has a critical role in the proliferation, survival and metastasis of several types of cancer. However, the molecular mechanisms through which PDI contributes to glioma remain unclear. Here, we aimed to investigate whether the differential expression of 17 PDI family members was closely related to the different clinicopathological features in gliomas from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas data sets. Additionally, four subgroups of gliomas (cluster 1/2/3/4) were identified based on consensus clustering of the PDI gene family. These findings not only demonstrated that a poorer prognosis, higher WHO grade, lower frequency of isocitrate dehydrogenase mutation and higher 1p/19q non‐codeletion status were significantly correlated with cluster 4 compared with the other clusters, but also indicated that the malignant progression of glioma was closely correlated with the expression of PDI family members. Moreover, we also constructed an independent prognostic marker that can predict the clinicopathological features of gliomas. Overall, the results indicated that PDI family members may serve as possible diagnostic markers in gliomas.

Background Glioblastoma (GBM) is the most common primary tumor in the brain, and the median survival time for GBM patients is only about 14 months; therefore, there is an urgent need for new and more effective strategies. Since cell cycle disorder is a key factor in tumor progression and immortalization, there is great potential for controlling cell cycle disorders in tumor cells in GBM patients. We began to study a novel combination of AQB and palbociclib to evaluate its potential as a new therapeutic target. Methods Protein mass spectrometry was used to identify the tumor suppressor genes up‐regulated by AQB.The effects of HOTAIR ‐ EZH2 inhibitor AQB and CDK4/6 inhibitor Palbociclib on glioma cells lines were examined in vitro and in vivo experiments. Results The combination of AQB and palbociclib inhibitors has a more pronounced suppression effect on the cell cycle, especially gliomas with high expression of HOTAIR and EZH2 and low expression of CWF19L1. We performed protein mass spectrometry to identify AQB upregulated tumor suppressor genes and confirmed that CWF19L1 is regulated by H3K27ac through chromatin immunoprecipitation‐quantitative PCR results. Univariate and multivariate Cox regression analysis and database analysis were performed to suggest CWF19L1 is a good prognostic factor. Our experimental results suggested that CWF19L1 can be significantly upregulated by AQB and lead to degradation of CDK4/6, resulting in G1 arrest. The combination of AQB and CDK4/6 inhibitor palbociclib is more effective in inhibiting the growth of glioma than in the single drug, both in vivo and in vitro. Similarly, we found that both AQB and palbociclib can inhibit Wnt/β‐catenin signaling, and the combined use of the two inhibitors has a stronger inhibitory effect on tumor metastasis. Conclusions The combination of AQB and CDK4/6 inhibitor palbociclib has been found to have significant antitumor effects, which is likely to become a new strategy for glioma treatment.