Switching Reaction Pathway of Medium-Concentration Ether Electrolytes to Achieve 4.5 V Lithium Metal Batteries.

Pursuing high-energy-density lithium metal batteries (LMBs) necessitates the advancement of electrolytes. Despite demonstrating high compatibility with lithium metal anodes (LMAs), ether-based electrolytes face challenges in achieving stable cycling at high voltages. Herein, we propose a strategy to enhance the high-voltage stability of medium-concentration (∼1 M) ether electrolytes by altering the reaction pathway of ether solvents. By employing a 1 M lithium difluoro(oxalato)borate in dimethoxyethane (LiDFOB/DME) electrolyte, we observed that LiDFOB displays a pronounced tendency for decomposition over DME, leading to a modification in the decomposition pathway of DME. This modification facilitates the formation of a stable organic-inorganic hybrid interface. Utilizing such an electrolyte, the Li-LCO cell demonstrates a discharge specific capacity of 146 mAh g-1 (5 C) and maintains retention of 86% over 1000 cycles at 2 C under a 4.5 V cutoff voltage. Additionally, the optimized ether electrolyte demonstrated outstanding cycling performance in Li-LCO full cells under practical conditions.

Nanophase-Separated, Elastic Epoxy Composite Thin Film as an Electrolyte for Stable Lithium Metal Batteries.

The design of solid polymer electrolytes (SPE) with high ionic conductivity and excellent mechanical properties is challenging because these two properties are often conflicting. To achieve both, a reaction-controlled strategy is proposed based on the nanophase separation of an ionic transport pathway and a supporting matrix to balance ionic mobility and mechanical properties. Specifically, an elastic epoxy polymer electrolyte (eEPE), synthesized via two-step polymerization, combines outstanding mechanical strength (toughness of 3.4 MJ m-3) and high ionic conductivity (3.5 × 10-4 S cm-1 at 25 °C). The nanostructured eEPE is both tough and flexible, therefore promotes uniform deposition of Li even under a high current density (2 mA cm-2 and 2 mAh cm-2). Importantly, eEPE composite films greatly improve the safety performance of the LiFePO4/Li pouch cells: safe operations are achieved under several abusive conditions. This work highlights an alternative route for high-safety solid-state lithium metal batteries of the next generation.

circ-Keratin 6c Promotes Malignant Progression and Immune Evasion of Colorectal Cancer through microRNA-485-3p/Programmed Cell Death Receptor Ligand 1 Axis.

Recently, circular RNA was reported to be a significant participant in the development of tumorigenesis, including colorectal cancer. Therefore, we aimed to clarify the precise role of circ-keratin 6C (circ-KRT6C) in colorectal cancer progression. The relative expression levels of circ-KRT6C, microRNA-485-3p (miR-485-3p), and programmed cell death receptor ligand 1 (PDL1) were analyzed by real-time quantitative polymerase chain reaction and Western blot assays. The proliferation was assessed by cell count kit 8 and colony-forming assays. The apoptotic cells were determined by flow cytometry assay. The migration and invasion were analyzed by transwell assay. Colorectal cancer cells were cocultured with peripheral blood mononuclear cells or cytokine-induced killer cells to assess immune response. The interaction relationships among circ-KRT6C, miR-485-3p, and PDL1 were examined by dual-luciferase reporter assay. The effects of circ-KRT6C inhibition in vivo were analyzed by an animal experiment. circ-KRT6C was overexpressed in colorectal cancer tissues and cells, and its level was associated with overall survival time of patients with colorectal cancer. The suppression of circ-KRT6C suppressed growth, migration, invasion, and immune escape while stimulating apoptosis in colorectal cancer cells, which was abolished by shortage of miR-485-3p. In addition, overexpression of miR-485-3p repressed malignant progression and immune evasion of colorectal cancer by targeting PDL1, implying that PDL1 was a functional target of miR-485-3p. A xenograft experiment also suggested that circ-KRT6C inhibition could repress tumor growth in vivo. circ-KRT6C could increase PDL1 expression by functioning as an miR-485-3p sponge, which promoted malignant progression and immune evasion of colorectal cancer cells. SIGNIFICANCE STATEMENT: circ-keratin 6c could increase programmed cell death receptor ligand 1 expression by functioning as a microRNA-16-5p sponge, which promoted malignant progression and immune evasion of colorectal cancer.

Exosomal circEPB41L2 serves as a sponge for miR-21-5p and miR-942-5p to suppress colorectal cancer progression by regulating the PTEN/AKT signalling pathway.

BACKGROUND: Exosomes contain many functional RNAs, including circular RNA (circRNA), which are critical for cancer progression. However, the role of exosomal circEPB41L2 in colorectal cancer (CRC) remains unclear. METHODS: Exosomes were isolated from plasma and cells. The characteristics of the exosomes were identified using transmission electron microscopy and nanoparticle tracking analysis. The protein levels of exosome markers and PTEN/AKT-related markers were measured using Western blot analysis. The expression of circEPB41L2, microRNA (miR)-21-5p and miR-942-5p was verified by quantitative real-time PCR. The proliferation, apoptosis, migration and invasion of cells were determined using cell counting kit eight assay, colony formation assay, flow cytometry, wound healing assay and transwell assay. Biotin-labelled RNA pull-down assay, dual-luciferase reporter assay and RIP assay were conducted to evaluate the interaction between circEPB41L2 and miR-21-5p or miR-942-5p. The effects of exosomal circEPB41L2 on colorectal cancer tumour growth were confirmed using animal experiments. RESULTS: CircEPB41L2 was downregulated in the exosomes from colorectal cancer patients and cells. Overexpressed circEPB41L2 inhibited colorectal cancer cell proliferation, migration, invasion and promoted apoptosis, as well as suppressed the activity of PTEN/AKT signalling pathway. CircEPB41L2 could sponge miR-21-5p or miR-942-5p. MiR-21-5p or miR-942-5p could reverse the inhibition effect of circEPB41L2 on colorectal cancer progression and PTEN/AKT signalling pathway. In addition, we discovered that circEPB41L2 was mainly located at exosomes. Exosomal circEPB41L2 also could restrain colorectal cancer progression and the activity of PTEN/AKT signalling pathway. Animal experiments suggested that exosomal-mediated circEPB41L2 inhibited colorectal cancer tumour growth. CONCLUSION: Our data revealed that exosomal circEPB41L2 sponged miR-21-5p and miR-942-5p to repress colorectal cancer progression by regulating the PTEN/AKT signalling pathway.

Circ-RNF121 regulates tumor progression and glucose metabolism by miR-1224-5p/FOXM1 axis in colorectal cancer.

AIM: Previous studies have reported that circular RNA (circRNA) is associated with the pathogenesis of CRC. This study was designed to reveal the mechanism of circ-ring finger protein 121 (circ-RNF121) in colorectal cancer (CRC). MATERIALS AND METHODS: The levels of circ-RNF121, microRNA-1224-5p (miR-1224-5p) and forkhead box M1 (FOXM1) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Protein level was detected by western blot. Cell proliferation was analyzed by 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and cell colony formation assays. Flow cytometry analysis was performed to investigate cell apoptosis. Cell migration and invasion were investigated by transwell and wound-healing assays. Cell glycolysis was detected using glucose, lactate and ADP/ATP ratio assay kits. The binding relationship between miR-1224-5p and circ-RNF121 or FOXM1 was predicted by starBase online database, and identified by dual-luciferase reporter assay. The impacts of circ-RNF121 silencing on tumor formation in vivo were disclosed by in vivo tumor formation assay. KEY FINDINGS: Circ-RNF121 and FOXM1 expression were dramatically upregulated, while miR-1224-5p expression was downregulated in CRC tissues or cells compared with control groups. Circ-RNF121 silencing repressed cell proliferation, migration, invasion and glycolysis but induced cell apoptosis in CRC, which were attenuated by miR-1224-5p inhibitor. Additionally, circ-RNF121 acted as a sponge of miR-1224-5p and miR-1224-5p bound to FOXM1. Circ-RNF121 silencing inhibited tumor growth in vivo. Furthermore, circ-RNF121 was secreted through being packaged into exosomes. SIGNIFICANCE: The finding provided a novel insight into studying circRNA-mediated CRC therapy.

METTL7B is a novel prognostic biomarker of lower-grade glioma based on pan-cancer analysis.

Methyltransferase-like 7B (METTL7B) is a member of the methyltransferase-like protein family that plays an important role in the development and progression of tumors. However, its prognostic value and the correlation of METTL7B expression and tumor immunity in some cancers remain unclear. By analyzing online data, we found that METTL7B is abnormally overexpressed in multiple human tumors and plays an important role in the overall survival (OS) of patients with 8 cancer types and disease-free survival (DFS) of patients with 5 cancer types. Remarkably, METTL7B expression was positively correlated with the OS and DFS of patients with lower-grade glioma (LGG). In addition, a positive correlation between METTL7B expression and immune cell infiltration in LGG was observed. Moreover, we identified a strong correlation between METTL7B expression and immune checkpoint gene expression in kidney chromophobe (KICH), LGG and pheochromocytoma and paraganglioma (PCPG). Furthermore, METTL7B was involved in the extracellular matrix (ECM) and immune-related pathways in LGGs. Finally, in vitro experiments showed that knockdown of METTL7B inhibited the growth, migration, invasion and the epithelial-mesenchymal transition (EMT) of LGG cells. METTL7B expression potentially represents a novel prognostic biomarker due to its significant association with immune cell infiltration in LGG.

Retracted: MicroRNA-495 Inhibits Gastric Cancer Cell Migration and Invasion Possibly via Targeting High Mobility Group AT-Hook 2 (HMGA2).

This publication has been retracted by the Editor due to the identification of non-original figure images and manuscript content that raise concerns regarding the credibility and originality of the study and the manuscript. Reference: Huashe Wang, Zhipeng Jiang, Honglei Chen, Xiaobin Wu, Jun Xiang, Junsheng Peng. MicroRNA-495 Inhibits Gastric Cancer Cell Migration and Invasion Possibly via Targeting High Mobility Group AT-Hook 2 (HMGA2). Med Sci Monit, 2017; 23: 640-648. DOI: 10.12659/MSM.898740.

Nitrofullerene, a C60-based Bifunctional Additive with Smoothing and Protecting Effects for Stable Lithium Metal Anode.

Practical applications of lithium metal anodes are gravely impeded by inhomogeneous lithium deposition, which results in dendrite growth. Electrolyte additives are proven to be effective in improving performance but usually serve only a single function. Herein, nitrofullerene is introduced as a bifunctional additive with a smoothing effect and forms a protective solid electrolyte interphase (SEI) layer on stable lithium metal anodes. By design, nitro-C60 can gather on electrode protuberances via electrostatic interactions and then be reduced to NO2- and insoluble C60. Next, the C60 anchors on the uneven groove of the lithium surface, resulting in a homogeneous distribution of Li ions. Finally, NO2- anions can react with metallic Li to build a compact and stable SEI with high ion transport. With a 5 mM nitro-C60 additive, Li-Li symmetric cells show superior cycle stability in both carbonate and ether electrolytes, Li-sulfur batteries with a high cathode loading (10.6 mg cm-2, 6 mAh cm-2) can achieve improved cycle retention of 63.2% over 100 cycles in a carbonate electrolyte, and full cells paired with a high-areal-capacity LiNi0.6Co0.2Mn0.2O2 cathode (3.5 mAh cm-2) exhibit a significantly enhanced cycle lifespan even under lean electrolyte conditions.

Analysis of TGCA data reveals genetic and epigenetic changes and biological function of MUC family genes in colorectal cancer.

Aim: Few studies focused on functions and regulatory networks of MUC family members in colorectal cancer based on comprehensive analysis of online database. Materials & methods: Copy number variation, methylation, pathway analysis and drug influence on MUC expression were analyzed based on The Cancer Genome Atlas and GTEx database. Results: Copy number variation analysis showed MUC heterozygous amplification and heterozygous deletion predominate. Methylation of MUC17, MUC12 and MUC4 were found related to gene expression. Function of MUC family genes mainly affects pathways such as apoptosis, cell cycle, DNA damage and EMT pathways. PLX4720, dabrafenib, gefitinib, afatinib and austocystin D can alter the expression of MUC gene. Conclusion: The genetic and epigenetic changes of MUC are related to the level of MUC expression in colorectal cancer.

Facile Generation of Polymer-Alloy Hybrid Layers for Dendrite-Free Lithium-Metal Anodes with Improved Moisture Stability.

Lithium-metal anodes are recognized as the most promising next-generation anodes for high-energy-storage batteries. However, lithium dendrites lead to irreversible capacity decay in lithium-metal batteries (LMBs). Besides, the strict assembly-environment conditions of LMBs are regarded as a challenge for practical applications. In this study, a workable lithium-metal anode with an artificial hybrid layer composed of a polymer and an alloy was designed and prepared by a simple chemical-modification strategy. Treated lithium anodes remained dendrite-free for over 1000 h in a Li-Li symmetric cell and exhibited outstanding cycle performance in high-areal-loading Li-S and Li-LiFePO4 full cells. Moreover, the treated lithium showed improved moisture stability that benefits from the hydrophobicity of the polymer, thus retaining good electrochemical performance after exposure to humid air.

De-identification of medical records using conditional random fields and long short-term memory networks.

The CEGS N-GRID 2016 Shared Task 1 in Clinical Natural Language Processing focuses on the de-identification of psychiatric evaluation records. This paper describes two participating systems of our team, based on conditional random fields (CRFs) and long short-term memory networks (LSTMs). A pre-processing module was introduced for sentence detection and tokenization before de-identification. For CRFs, manually extracted rich features were utilized to train the model. For LSTMs, a character-level bi-directional LSTM network was applied to represent tokens and classify tags for each token, following which a decoding layer was stacked to decode the most probable protected health information (PHI) terms. The LSTM-based system attained an i2b2 strict micro-F1 measure of 0.8986, which was higher than that of the CRF-based system.

Building a comprehensive syntactic and semantic corpus of Chinese clinical texts.

OBJECTIVE: To build a comprehensive corpus covering syntactic and semantic annotations of Chinese clinical texts with corresponding annotation guidelines and methods as well as to develop tools trained on the annotated corpus, which supplies baselines for research on Chinese texts in the clinical domain. MATERIALS AND METHODS: An iterative annotation method was proposed to train annotators and to develop annotation guidelines. Then, by using annotation quality assurance measures, a comprehensive corpus was built, containing annotations of part-of-speech (POS) tags, syntactic tags, entities, assertions, and relations. Inter-annotator agreement (IAA) was calculated to evaluate the annotation quality and a Chinese clinical text processing and information extraction system (CCTPIES) was developed based on our annotated corpus. RESULTS: The syntactic corpus consists of 138 Chinese clinical documents with 47,426 tokens and 2612 full parsing trees, while the semantic corpus includes 992 documents that annotated 39,511 entities with their assertions and 7693 relations. IAA evaluation shows that this comprehensive corpus is of good quality, and the system modules are effective. DISCUSSION: The annotated corpus makes a considerable contribution to natural language processing (NLP) research into Chinese texts in the clinical domain. However, this corpus has a number of limitations. Some additional types of clinical text should be introduced to improve corpus coverage and active learning methods should be utilized to promote annotation efficiency. CONCLUSIONS: In this study, several annotation guidelines and an annotation method for Chinese clinical texts were proposed, and a comprehensive corpus with its NLP modules were constructed, providing a foundation for further study of applying NLP techniques to Chinese texts in the clinical domain.

MicroRNA-495 Inhibits Gastric Cancer Cell Migration and Invasion Possibly via Targeting High Mobility Group AT-Hook 2 (HMGA2).

BACKGROUND Gastric cancer is one of the most common malignancies, and has a high mortality rate. miR-495 acts as a suppressor in some cancers and HMGA2 (high mobility group AT-hook 2) is a facilitator for cell growth and epithelial-mesenchymal transition (EMT), but little is known about their effect in gastric cancer. This study aimed to investigate the role and mechanism of miR-495 in gastric cancer. MATERIAL AND METHODS miR-495 levels were quantitatively analyzed in gastric cancer tissue and GES-1, SGC-7901, BGC-823, and HGC-27 cell lines by qRT-PCR. Levels of miR-495 and HMGA2 were altered by cell transfection, after which cell migration and invasion were examined by Transwell and E-cadherin (CDH1); vimentin (VIM), and alpha smooth muscle actin (ACTA2) were detected by qRT-PCR and Western blotting. The interaction between miR-495 and HMGA2 was verified by dual-luciferase reporter assay. RESULTS miR-495 was significantly downregulated in cancer tissue and cell lines (p<0.05). Its overexpression inhibited cell migration and invasion, elevated CDH1, and inhibited VIM and ACTA2 levels in BGC-823 and HGC-27 cells. miR-495 directly inhibited HMGA2, which was upregulated in gastric cancer tissue, and promoted cell migration and invasion, inhibited CDH1, and elevated VIM and ACTA2. CONCLUSIONS miR-495 acts as a tumor suppressor in gastric cancer by inhibiting cell migration and invasion, which may be associated with its direct inhibition on HMGA2. These results suggest a promising therapeutic strategy for gastric cancer treatment.

Serum microRNA-145 as a novel biomarker in human ovarian cancer.

Ovarian cancer is one of the most threatening diseases among women in the world. Current detection methods are expensive and lack accuracy. Thus, a fast, non-invasive biomarker for detecting ovarian cancer is urgently needed. Compelling evidences have been demonstrated that microRNAs, a large family of single-stranded and non-protein-coding RNA molecules, can serve as useful biomarkers in cancer detection. In this study, the relative expressions of microRNA-145 (miR-145) in the serum of patients with ovarian cancer and healthy controls were investigated in an independent study. Subsequently, the diagnosis and prognosis value of miR-145 as a biomarker for ovarian cancer were examined. Furthermore, we performed a meta-analysis to summarize all the results from published studies and this study. Relative expressions of miR-145 were investigated in three independent groups (malignant ovarian cancer, benign ovarian tumor, and healthy controls), comprising a total of 270 participants. Receiver operating characteristic (ROC) curves and overall survival (OS) curves were conducted to compare miR-145 level and clinical characteristics among the three groups. The results showed that relative expressions of the serum miR-145 were significantly down-regulated in patients with malignant ovarian cancer and benign ovarian cancer, compared to healthy controls (P < 0.01). Serum miR-145 levels could discriminate patients with malignant ovarian cancer from healthy controls, with a power area under the curve (AUC) of 0.82 (95 % confidence interval (CI) = 0.77-0.88). Furthermore, patients with low serum levels of miR-145 had a significantly shorter median overall survival rate (hazard ratio (HR) = 1.81, 95 % CI = 1.03-3.17, P = 0.039). The meta-analysis yields good diagnostic performances of miR-145 in various cancers, with an AUC of 0.82 (95 % CI, 0.78-0.85). In conclusion, the present study suggested that miR-145 can potentially serve as an outstanding biomarker for ovarian and other human cancers detection.

LPS preconditioning ameliorates intestinal injury in a rat model of hemorrhagic shock.

OBJECTIVE AND DESIGN: Previous studies indicate that endotoxin preconditioning may decrease the inflammatory response and alleviate intestinal mucosal damage caused by sepsis. However, it is not known whether preconditioning with endotoxin might protect the intestinal mucosa after hemorrhagic shock. In this study, we investigated the effect of lipopolysaccharide (LPS) preconditioning on the intestinal mucosa following hemorrhagic shock in a rat model. Given that intestinal toll-like receptor 4 (TLR4) signaling is exaggerated in response to LPS, we further investigated the role of TLR4 signaling in endotoxin tolerance. METHODS: Animals were pre-treated with intra-peritoneal Escherichia coli LPS for 5 days prior to hemorrhagic shock. Animals were bled to achieve a mean arterial pressure (MAP) of 35-40 mmHg, then resuscitated with Ringer solution and the heparinized shed blood to maintain MAP between 90 and 100 mmHg. The distal ileum was harvested after resuscitation and graded for mucosal damage. TNF-α, TLR4, cleaved caspase-3, and intestinal trefoil factor 3 (TFF3) levels were measured at different time points. RESULTS: Pretreatment with LPS significantly reduced intestinal mucosal damage and protein levels of cleaved caspase-3. Furthermore, animals pre-treated with LPS experienced reduction of TNF-α and increased mucosal expression of TFF3. LPS tolerance was associated with reduced TLR4 expression. CONCLUSIONS: Endotoxin preconditioning can lessen the effects of ischemia and reperfusion injury in intestinal mucosa of a rat model with hemorrhagic shock. It is hypothesized that this effect is mediated via inhibition of TLR4 over-expression.

Fullerenol as a nano-molecular sieve additive enables stable zinc metal anodes.

Aqueous zinc batteries (AZBs) with the advantages of safety, low cost, and sustainability are promising candidates for large-scale energy storage devices. However, the issues of interface side reactions and dendrite growth at the zinc metal anode (ZMA) significantly harm the cycling lifespan of AZBs. In this study, we designed a nano-molecular sieve additive, fullerenol (C60(OH)n), which possesses a surface rich in hydroxyl groups that can be uniformly dispersed in the aqueous solution, and captures free water in the electrolyte, thereby suppressing the occurrence of interfacial corrosion. Besides, fullerenol can be further reduced to fullerene (C60) on the surface of ZMA, holding a unique self-smoothing effect that can inhibit the growth of dendritic Zn. With the synergistic action of these two effects, the fullerenol-contained electrolyte (FE) enables dendrite-free ZMAs. The Zn-Ti half-cell using FE exhibits stable cycling over 2500 times at 5 mA cm-2 with an average Coulombic efficiency as high as 99.8 %. Additionally, the Zn-NaV3O8 cell using this electrolyte displays a capacity retention rate of 100 % after 1000 cycles at -20 °C. This work provides important insights into the molecular design of multifunctional electrolyte additives.

Stable cyclic ether as an electrolyte additive for high-performance lithium metal batteries.

Introducing a methyl group into 1,3-dioxolane (DOL) to obtain a stable cyclic ether, 4-methyl-1,3-dioxolane (4-Me DOL), allows it to be used as an additive in LiPF6-based carbonate electrolytes. The addition of 4-Me DOL can form a stable SEI with good Li+ transport ability, which can simultaneously improve the rate capability and cycling performance of lithium metal batteries.

Identification of Anoikis-Related Genes in Spinal Cord Injury: Bioinformatics and Experimental Validation.

Spinal cord injury (SCI) is a serious disease without effective therapeutic strategies. To identify the potential treatments for SCI, it is extremely important to explore the underlying mechanism. Current studies demonstrate that anoikis might play an important role in SCI. In this study, we aimed to identify the key anoikis-related genes (ARGs) providing therapeutic targets for SCI. The mRNA expression matrix of GSE45006 was downloaded from the Gene Expression Omnibus (GEO) database, and the ARGs were downloaded from the Molecular Signatures Database (MSigDB database). Then, the potential differentially expressed ARGs were identified. Next, correlation analysis, gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and protein-protein interaction (PPI) analysis were employed for the differentially expressed ARGs. Moreover, miRNA-gene networks were constructed by the hub ARGs. Finally, RNA expression of the top ten hub ARGs was validated in the SCI cell model and rat SCI model. A total of 27 common differentially expressed ARGs were identified at different time points (1, 3, 7, and 14 days) following SCI. The GO and KEGG enrichment analysis of these ARGs indicated several enriched terms related to proliferation, cell cycle, and apoptotic process. The PPI results revealed that most of the ARGs interacted with each other. Ten hub ARGs were further screened, and all the 10 genes were validated in the SCI cell model. In the rat model, only seven genes were validated eventually. We identified 27 differentially expressed ARGs of the SCI through bioinformatic analysis. Seven real hub ARGs (CCND1, FN1, IGF1, MYC, STAT3, TGFB1, and TP53) were identified eventually. These results may expand our understanding of SCI and contribute to the exploration of potential SCI targets.

Integrated profiling identifies ferredoxin 1 as an immune-related biomarker of malignant phenotype in glioma.

Background: Glioma, a highly resistant and recurrent type of central nervous system tumor, poses a significant challenge in terms of effective drug treatments and its associated mortality rates. Despite the discovery of Ferredoxin 1 (FDX1) as a crucial participant in cuproptosis, an innovative mechanism of cellular demise, its precise implications for glioma prognosis and tumor immune infiltration remain inadequately elucidated. Methods: To analyze pan-cancer data, we employed multiple public databases. Gene expression evaluation was performed using tissue microarray (TMA) and single-cell sequencing data. Furthermore, four different approaches were employed to assess the prognostic importance of FDX1 in glioma. We conducted the analysis of differential expression genes (DEGs) and Gene Set Enrichment Analysis (GSEA) to identify immune-related predictive signaling pathways. Somatic mutations were assessed using Tumor Mutation Burden (TMB) and waterfall plots. Immune cell infiltration was evaluated with five different algorithms. Furthermore, we performed in vitro investigations to evaluate the biological roles of FDX1 in glioma. Results: Glioma samples exhibited upregulation of FDX1, which in turn predicted poor prognosis and was positively associated with unfavorable clinicopathological characteristics. Notably, the top four enriched signaling pathways were immune-related, and the discovery revealed a connection between the expression of FDX1 and the frequency of mutations or the TMB. The FDX1_high group exhibited heightened infiltration of immune cells, and there existed a direct association between the expression of FDX1 and the regulation of immune checkpoint. In vitro experiments demonstrated that FDX1 knockdown reduced proliferation, migration, invasion and transition from G2 to M phase in glioma cells. Conclusion: In glioma, FDX1 demonstrated a positive association with the advancement of malignancy and changes in the infiltration of immune cells.