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Background: Numerous studies have shown a strong correlation between disulfidptosis and various cancers. However, the expression and function of RPN1, a crucial gene in disulfidptosis, remain unclear in the context of cancer. Methods: Gene expression and clinical information on lung adenocarcinoma were obtained from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases. RPN1 expression was analyzed using the Timer2.0 and the Human Protein Atlas (HPA) databases. Prognostic significance was assessed using Cox regression analysis and Kaplan-Meier curves. Genetic mutations and methylation levels were examined using the cBioPortal and UALCAN platforms, respectively. The relationship between RPN1 and tumor mutation burden (TMB) and microsatellite instability (MSI) across different cancer types was analyzed using the Spearman correlation coefficient. The relationship between RPN1 and immune cell infiltration was analyzed using the Timer2.0 database, whereas variations in drug sensitivity were explored using the CellMiner database. Receiver operating characteristic curves validated RPN1's diagnostic potential in glioma, and its correlation with immune checkpoint inhibitors (ICIs) was assessed using Spearman's correlation coefficient. Single-sample gene set enrichment analysis elucidated a link between RPN1 and immune cells and pathways. In addition, a nomogram based on RPN1 was developed to predict patient prognosis. The functional impact of RPN1 on glioma cells was confirmed using scratch and Transwell assays. Result: RPN1 was aberrantly expressed in various cancers and affected patient prognosis. The main mutation type of RPN1 in the cancer was amplified. RPN1 exhibited a positive correlation with myeloid-derived suppressor cells, neutrophils, and macrophages, and a negative correlation with CD8+ T cells and hematopoietic stem cells. RPN1 expression was associated with TMB and MSI in various cancers. The expression of RPN1 affected drug sensitivity in cancer cells. RPN1 was positively correlated with multiple ICIs in gliomas. RPN1 also affected immune cell infiltration into the tumor microenvironment. RPN1 was an independent prognostic factor for gliomas, and the nomogram demonstrated excellent predictive performance. Interference with RPN1 expression reduces the migratory and invasive ability of glioma cells. Conclusion: RPN1 exerts multifaceted effects on different stages of cancer, including immune infiltration, prognosis, and treatment outcomes. RPN1 expression affects the prognosis and immune microenvironment infiltration in patients with glioma, making RPN1 a potential target for the treatment of glioma.
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BACKGROUND: The study aimed to investigate the role of copper death-related genes (CRGs) in bladder cancer (BC) for improved prognosis assessment. METHODS: Multi-omics techniques were utilized to analyze CRG expression in BC tissues from TCGA and GEO databases. Consensus clustering categorized patients into molecular subtypes based on clinical characteristics and immune cell infiltration. RESULTS: An innovative risk assessment model identified eight critical genes associated with BC risk. In vitro and in vivo experiments validated LIPT1's significant impact on copper-induced cell death, proliferation, migration, and invasion in BC. CONCLUSION: This multi-omics analysis elucidates the pivotal role of CRGs in BC progression, suggesting enhanced risk assessment through molecular subtype categorization and identification of key genes like LIPT1. Insights into these mechanisms offer the potential for improved diagnosis and treatment strategies for BC patients.
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BACKGROUND: The nck-associated protein 1 (NCKAP1) of the disulfidptosis-related gene is essential in programmed cell death. However, a comprehensive analysis of the biological significance of NCKAP1 in pan-cancer is lacking. METHODS: Gene expression matrices and clinical expression information of cancers were obtained from The Cancer Genome Atlas (TCGA) and Genotype Tissue Expression (GTEX) databases. A comprehensive analysis of NCKAP1 expression, biological function, gene mutation, immune cell infiltration, DNA methylation, and drug sensitivity profiles in pan-cancer was performed using the Timer2.0, HPA, GEPIA, STRING, cBioPortal, UALCAN and CellMiner databases. The prognostic value of NCKAP1 was investigated based on COX regression analysis and the Kaplan-Meier(K-M) curves. A nomogram was established to verify the clinical value of NCKAP1 for LUAD. The correlation between NCKAP1 and immune cells and signaling pathways were investigated by single-sample gene set enrichment analysis(ssGSEA). Validation was performed using PCR, Western Blot (WB), and Transwell assays. RESULT: Significant differences in expression levels, mutation levels, and methylation levels of NCKAP1 between tumor and normal samples. NCKAP1 affects the prognosis of various cancers. NCKAP1 is strongly associated with microsatellite instability (MSI) and tumor mutational burden (TMB). The Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicate that NCKAP1 is strongly associated with cell death and tumor immunity. The expression of NCKAP1 affects the sensitivity to various drugs. Moreover, NCKAP1 is an independent predictor of prognosis in LUAD patients. The results of ssGSEA showed that elevated NCKAP1 expression was positively correlated with multiple immune-related signaling pathways. PCR analysis showed that the expression of NCKAP1 was increased in LUAD cells. Transwell invasion assay showed that overexpression of NCKAP1 resulted in enhanced invasion of LUAD cells. CONCLUSIONS: We comprehensively analyzed the relationship between NCKAP1 and pan-cancer and its potential clinical value. NCKAP1 could be a potential immune marker for various cancers (especially LUAD), providing new insights and insights for cancer therapy.
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Background: Lung cancer continues to be a problem faced by all of humanity. It is the cancer with the highest morbidity and mortality in the world, and the most common histological type of lung cancer is lung adenocarcinoma (LUAD), accounting for about 40% of lung malignant tumors. This study was conducted to discuss and explore the immune-related biomarkers and pathways during the development and progression of LUAD and their relationship with immunocyte infiltration. Methods: The cohorts of data used in this study were downloaded from the Gene Expression Complex (GEO) database and the Cancer Genome Atlas Program (TCGA) database. Through the analysis of differential expression analysis, weighted gene co-expression network analysis (WGCNA), and least absolute shrinkage and selection operator(LASSO), selecting the module with the highest correlation with LUAD progression, and then the HUB gene was further determined. The Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were then used to study the function of these genes. Single-sample GSEA (ssGSEA) analysis was used to investigate the penetration of 28 immunocytes and their relationship with HUB genes. Finally, the receiver operating characteristic curve (ROC) was used to evaluate these HUB genes accurately to diagnose LUAD. In addition, additional cohorts were used for external validation. Based on the TCGA database, the effect of the HUB genes on the prognosis of LUAD patients was assessed using the Kaplan-Meier curve. The mRNA levels of some HUB genes in cancer cells and normal cells were analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Results: The turquoise module with the highest correlation with LUAD was identified among the seven modules obtained with WGCNA. Three hundred fifty-four differential genes were chosen. After LASSO analysis, 12 HUB genes were chosen as candidate biomarkers for LUAD expression. According to the immune infiltration results, CD4 + T cells, B cells, and NK cells were high in LUAD sample tissue. The ROC curve showed that all 12 HUB genes had a high diagnostic value. Finally, the functional enrichment analysis suggested that the HUB gene is mainly related to inflammatory and immune responses. According to the RT-qPCR study, we found that the expression of DPYSL2, OCIAD2, and FABP4 in A549 was higher than BEAS-2B. The expression content of DPYSL2 was lower in H1299 than in BEAS-2B. However, the expression difference of FABP4 and OCIAD2 genes in H1299 lung cancer cells was insignificant, but both showed a trend of increase. Conclusions: The mechanism of LUAD pathogenesis and progression is closely linked to T cells, B cells, and monocytes. 12 HUB genes(ADAMTS8, CD36, DPYSL2, FABP4, FGFR4, HBA2, OCIAD2, PARP1, PLEKHH2, STX11, TCF21, TNNC1) may participate in the progression of LUAD via immune-related signaling pathways.
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Exploring the topological surface state of a topological semimetal by the transport technique has always been a big challenge because of the overwhelming contribution of the bulk state. In this work, we perform systematic angular-dependent magnetotransport measurements and electronic band calculations on SnTaS2 crystals, a layered topological nodal-line semimetal. Distinct Shubnikov-de Haas quantum oscillations were observed only in SnTaS2 nanoflakes when the thickness was below about 110 nm, and the oscillation amplitudes increased significantly with decreasing thickness. By analysis of the oscillation spectra, together with the theoretical calculation, a two-dimensional and topological nontrivial nature of the surface band is unambiguously identified, providing direct transport evidence of drumhead surface state for SnTaS2. Our comprehensive understanding of the Fermi surface topology of the centrosymmetric superconductor SnTaS2 is crucial for further research on the interplay of superconductivity and nontrivial topology.
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van der Waals (vdW) heterodiodes composed of two-dimensional (2D) layered materials led to a new prospect in photoelectron diodes and photovoltaic devices. Existing studies have shown that Type-I heterostructures have great potential to be used as photodetectors; however, the tunneling phenomena in Type-I heterostructures have not been fully revealed. Herein, a highly efficient nn+ WS2/PtS2 Type-I vdW heterostructure photodiode is constructed. The device shows an ultrahigh reverse rectification ratio of 105 owing to the transmission barrier-induced low reverse current. A unilateral depletion region is formed on WS2, which inhibits the recombination of carriers at the interface and makes the external quantum efficiency (EQE) of the device reach 67%. Due to the tunneling mechanism of the device, which allows the co-existence of a large photocurrent and a low dark current, this device achieves a light on/off ratio of over 105. In addition, this band design allows the device to maintain a high detectivity of 4.53 × 1010 Jones. Our work provides some new ideas for exploring new high-efficiency photodiodes.
