Pan-analysis reveals CACYBP to be a novel prognostic and predictive marker for multiple cancers
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ABSTRACT:
SUBMITTER: Mo B
PROVIDER: S-EPMC10839390 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:Background: Coronavirus disease 2019 (COVID-19) has been a public threat and healthcare concern caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. During the period of the pandemic of COVID-19, cancer patients should be paid more attention as more severe events are found in cancer patients infected with SARS-CoV-2. Basigin (BSG) is an essential factor for the infection and progression of COVID-19 and tumorigenesis of multiple tumors, which may serve as a novel target for the effective treatment against COVID-19 and multiple human cancers. Methods: A total of 19,020 samples from multiple centers were included in our research for the comprehensive investigation of the differences in BSG expression among human organs, cancer cells, cancer tissues, and normal tissues. Cox regression analysis and Kaplan-Meier curves were utilized to explore the prognosis factor of BSG in cancers. Correlation analyses were used to determine associations of BSG expression with tumor mutational burden, the immune microenvironment, etc. Gene set enrichment analysis was applied to explore the underlying mechanisms of BSG in cancers. Results: Compared with normal tissues, BSG expression was high in 13 types of cancers (cholangiocarcinoma, etc.) and low in colon adenocarcinoma and rectum adenocarcinoma. BSG expression was related to the prognosis of eight cancers (e.g., invasive breast carcinoma) (p < 0.05). The gene also demonstrated a pronounced effect in identifying 12 cancers (cholangiocarcinoma, etc.) from their control samples (AUC >0.7). The BSG expression was associated with DNA methyltransferases, mismatch repair genes, immune infiltration levels, tumor mutational burden, microsatellite instability, neoantigen, and immune checkpoints, suggesting the potential of BSG as an exciting target for cancer treatment. BSG may play its role in several cancers by affecting several signaling pathways such as drug cytochrome metabolism P450 and JAK-STAT. Conclusion: BSG may be a novel biomarker for treating and identifying multiple human cancers.
| S-EPMC9136262 | biostudies-literature
Project description:Despite many striking connections, the biological similarities between embryonic development and tumorigenesis have not been well explored. Development of the placental villi is a crucial process involving many cellular activities, including immunity, proliferation, and cell adhesion. In this study, we designed a strategy to identify the gene expression pattern of villi development and to explore the corresponding features in tumors. We discovered villi-specific genes that are highly expressed in the villus as opposed to the mature placenta and then measured the expression levels of these genes in tumors. We found large changes in the expression of villi-specific genes in multiple types of cancer. These villi-specific genes showed distinct expression patterns and were primarily involved in three biological processes: immune-related (5), proliferation-related (6), and focal adhesion-related (8); these genes were extracted from the corresponding enriched Gene Ontology (GO) terms. We observed that these genes were also dysregulated at the transcriptional level across several tumor types. Moreover, the expression of these three gene groups was associated with poor prognosis in a subset of tumors. Based on villi-specific gene expression, this correlation study indicated the existence of common gene expression patterns between embryonic development and tumorigenesis. Therefore, a systematic analysis of villi-specific gene aberrations in various tumors could serve as an indicator for identifying novel prognostic biomarkers.
| S-EPMC5604211 | biostudies-literature
Project description:Methyltransferase-like protein 7A (METTL7A) is an m6A RNA methyltransferase that has been linked to cancer prognosis and drug resistance. However, a comprehensive analysis of METTL7A is lacking. The expression of METTL7A, prognostic performance, correlation with microsatellite instability (MSI), tumor mutational burden (TMB), and immune infiltration was investigated in The Cancer Genome Atlas (TCGA). Immunohistochemistry staining was applied to detect METTL7A in 6 tumors. METTL7A was significantly decreased in 19 cancers in TCGA including LUAD. Alterations of METTL7A include amplification and mutation, and epigenetic alterations revealed increased promoter methylation may result in down-regulation of METTL7A in LUAD. We also found that METTL7A was linked to both TMB and MSI in LUAD. METTL7A was increasingly correlated with invasive immune cells, while being negatively associated with Macrophages M0, Mast cells activated, activated memory CD4 T cells, CD8 T cells, and follicular helper T cells in several tumors. Additionally, METTL7A showed similar correlation with immune therapy-related genes across cancers. Our biological validation found that the protein levels of METTL7A were down-regulated in breast cancer (BRCA), endometrioid cancer (UCEC), colon cancer (COAD), prostate cancer (PRAD), and kidney clear cell carcinoma (KIRC), as detected by immunohistochemistry staining. Overall, our work indicates that METTL7A may serve as promising diagnostic and prognostic indicator of LUAD, and our work sheds light on the potential immunological and prognostic roles of METTL7A in human cancers.
| S-EPMC10859372 | biostudies-literature
Project description:Introduction: Several recent studies pointed out that chromodomain-helicase-DNA-binding protein 1-like (CHD1L) is a putative oncogene in many human tumors. However, up to date, there is no pan-cancer analysis performed to study the different aspects of this gene expression and behavior in tumor tissues. Methods: Here, we applied several bioinformatics tools to make a comprehensive analysis for CHD1L. Firstly we assessed the expression of CHD1L in several types of human tumors and tried to correlate that with the stage and grade of the analyzed tumors. Following that, we performed a survival analysis to study the correlation between CHD1L upregulation in tumors and the clinical outcome. Additionally, we investigated the mutation forms, the correlation with several immune cell infiltration, and the potential molecular mechanisms of CHD1L in the tumor tissue. Result and discussion: The results demonstrated that CHD1L is a highly expressed gene across several types of tumors and that was correlated with a poor prognosis for most cancer patients. Moreover, it was found that CHD1L affects the tumor immune microenvironment by influencing the infiltration level of several immune cells. Collectively, the current study provides a comprehensive overview of the oncogenic roles of CHD1L where our results nominate CHD1L as a potential prognostic biomarker and target for antitumor therapy development.
| S-EPMC10076660 | biostudies-literature
Project description:Aldolase B (ALDOB) gene is essential for the process of glycolysis and differentially expressed in cancers. The aims of this study were to explore the potential role of ALDOB in pan-cancer, in order to deepen the research on the pathological mechanism of cancer. Hence, we used several online tools (TIMER2, GEPIA2, UALCAN, cBioPortal, and MXPRESS) and R language to identify the correlation between the ALDOB expression and survival analysis, genetic alteration, DNA methylation, and immune cell infiltration based on The Cancer Genome Atlas project. The results showed that ALDOB was lowly expressed in pan-cancer. Survival analysis revealed that low expression of ALDOB was markedly related with poor clinical prognosis, while the genetic alteration within ALDOB changed along with the difference of overall survival (OS) and disease-free survival (DFS) prognosis in several cancers. A possible relationship between DNA methylation and ALDOB expression for several tumors was found. Besides, ALDOB expression was confirmed to be associated with tumor immune cell infiltration, especially in breast invasive carcinoma (BRCA), esophageal carcinoma (ESCA), and testicular germ cell tumors (TGCT) cases. Further, the enrichment analysis demonstrated that metabolic pathway was closely related to ALDOB expression. Our results provide a comprehensive pan-cancer analysis and suggest ALDOB could act as a promising tumor predictive biomarker for human cancer.
| S-EPMC10118374 | biostudies-literature
Project description:BackgroundDigestive system cancers pose a significant global health challenge with high incidence and mortality rates. Inflammation is a key factor in cancer progression, necessitating reliable prognostic indicators. The pan-immune-inflammation value (PIV), as a new biomarker of immune-inflammatory response, has emerged as a potential prognostic biomarker for cancers.MethodsWe performed a meta-analysis to evaluate the prognostic significance of PIV in digestive system cancers. Our search, up to June 2024, included 20 studies from 19 articles with 5037 patients. We extracted and analyzed data on PIV levels and assessed hazard ratios (HRs) for overall survival (OS), progression-free survival (PFS), disease-free survival (DFS), recurrence-free survival (RFS), and cancer-specific survival (CSS) using STATA 14.0.ResultsOur analysis found that high PIV levels were significantly associated with poor prognosis in patients with digestive system cancers. Specifically, high PIV was linked to shorter OS (HR = 2.039, P < 0.001), PFS (HR = 1.877, P = 0.028), DFS (HR = 1.624, P = 0.005), RFS (HR = 2.393, P = 0.037), and CSS (HR = 2.053, P < 0.001). Additionally, the adverse prognostic impact of high PIV on OS was consistent across different cancer types, including digestive tract, colorectal, esophageal, and hepatobiliary pancreatic cancers. Although some heterogeneity was observed, sensitivity and bias analyses confirmed the reliability of these findings.ConclusionsPIV was a valuable and practical prognostic marker for digestive system cancers, providing significant predictive value across multiple survival metrics. Its simplicity and minimal invasiveness nature support its potential integration into routine clinical practice.
| S-EPMC11577901 | biostudies-literature
Project description:BackgroundCentrosomal protein 55 (CEP55) plays a significant role in specific cancers. However, comprehensive research on CEP55 is lacking in pan-cancer.MethodsIn-house and multi-center samples (n = 15,823) were used to analyze CEP55 in 33 cancers. The variance of CEP55 expression levels among tumor and control groups was evaluated by the Wilcoxon rank-sum test and standardized mean difference (SMD). The clinical value of CEP55 in cancers was assessed using receiver operating characteristic (ROC) curves, Cox regression analysis, and Kaplan-Meier curves. The correlations between CEP55 expression and the immune microenvironment were explored using Spearman's correlation coefficient.ResultsThe data of clustered regularly interspaced short palindromic repeats confirmed that CEP55 was essential for the survival of cancer cells in multiple cancer types. Elevated CEP55 mRNA expression was observed in 20 cancers, including glioblastoma multiforme (p < 0.05). CEP55 mRNA expression made it feasible to distinguish 21 cancer types between cancer specimens and their control samples (AUC = 0.97), indicating the potential of CEP55 for predicting cancer status. Overexpression of CEP55 was correlated with the prognosis of cancer individuals for 18 cancer types, exhibiting its prognostic value. CEP55 expression was relevant to tumor mutation burden, microsatellite instability, neoantigen counts, and the immune microenvironment in various cancers (p < 0.05). The expression level and clinical relevance of CEP55 in cancers were verified in lung squamous cell carcinoma using in-house and multi-center samples (SMD = 4.07; AUC > 0.95; p < 0.05).ConclusionCEP55 may be an immune-related predictive and prognostic marker for multiple cancers, including lung squamous cell carcinoma.
| S-EPMC10182662 | biostudies-literature
Project description:PTBP1 is an oncogene that regulates the splicing of precursor mRNA. However, the relationship between PTBP1 expression and gene methylation, cancer prognosis, and tumor microenvironment remains unclear. The expression profiles of PTBP1 across various cancers were derived from the TCGA, as well as the GTEx and CGGA databases. The CGGA mRNA_325, CGGA mRNA_301, and CGGA mRNA_693 datasets were utilized as validation cohorts. Immune cell infiltration scores were approximated using the TIMER 2.0 tool. Functional enrichment analysis for groups with high and low PTBP1 expression was conducted using Gene Set Enrichment Analysis (GSEA). Methylation data were predominantly sourced from the SMART and Mexpress databases. Linked-omics analysis was employed to perform functional enrichment analysis of genes related to PTBP1 methylation, as well as to conduct protein functional enrichment analysis. Single-cell transcriptome analysis and spatial transcriptome analysis were carried out using Seurat version 4.10. Compared to normal tissues, PTBP1 is significantly overexpressed and hypomethylated in various cancers. It is implicated in prognosis, immune cell infiltration, immune checkpoint expression, genomic variation, tumor neoantigen load, and tumor mutational burden across a spectrum of cancers, with particularly notable effects in low-grade gliomas. In the context of gliomas, PTBP1 expression correlates with WHO grade and IDH1 mutation status. PTBP1 expression and methylation play an important role in a variety of cancers. PTBP1 can be used as a marker of inflammation, progression and prognosis in gliomas.
| S-EPMC11199703 | biostudies-literature
Project description:The DEAD-box RNA helicase (DDX) family plays a critical role in the growth and development of multiple organisms. DDX1 is involved in mRNA/rRNA processing and mature, virus replication and transcription, hormone metabolism, tumorigenesis, and tumor development. However, how DDX1 functions in various cancers remains unclear. Here, we explored the potential oncogenic roles of DDX1 across 33 tumors with The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) databases. DDX1 is highly expressed in breast cancer (BRCA), cholangiocarcinoma (CHOL), and colon adenocarcinoma (COAD), but it is lowly expressed in renal cancers, including kidney renal clear cell carcinoma (KIRC), kidney chromophobe (KICH), and kidney renal papillary cell carcinoma (KIRP). Low expression of DDX1 in KIRC is correlated with a good prognosis of overall survival (OS) and disease-free survival (DFS). Highly expressed DDX1 is linked to a poor prognosis of OS for adrenocortical carcinoma (ACC), bladder urothelial carcinoma (BLCA), KICH, and liver hepatocellular carcinoma (LIHC). Also, the residue Ser481 of DDX1 had an enhanced phosphorylation level in BRCA and ovarian cancer (OV) but decreased in KIRC. Immune infiltration analysis exhibited that DDX1 expression affected CD8+ T cells, and it was significantly associated with MSI (microsatellite instability), TMB (tumor mutational burden), and ICT (immune checkpoint blockade therapy) in tumors. In addition, the depletion of DDX1 dramatically affected the cell viability of human tumor-derived cell lines. DDX1 could affect the DNA repair pathway and the RNA transport/DNA replication processes during tumorigenesis by analyzing the CancerSEA database. Thus, our pan-cancer analysis revealed that DDX1 had complicated impacts on different cancers and might act as a prognostic marker for cancers such as renal cancer.Supplementary informationThe online version contains supplementary material available at 10.1007/s43657-021-00034-x.
| S-EPMC9590584 | biostudies-literature
Project description:BackgroundDespite accumulating evidence revealing that Glucose-6-phosphate dehydrogenase (G6PD) is highly expressed in many tumor tissues and plays a remarkable role in cancer tumorigenesis and progression, there is still a lack of G6PD pan-cancer analysis. This study was designed to analyze the expression status and prognostic significance of G6PD in pan-cancer.MethodsG6PD expression data were obtained from multiple data resources including the Genotype-Tissue Expression, the Cancer Genome Atlas, and the Tumor Immunity Estimation Resource. These data were used to assess the G6PD expression, prognostic value, and clinical characteristics. The ESTIMATE algorithms were used to analyze the association between G6PD expression and immune-infiltrating cells and the tumor microenvironment. The functional enrichment analysis was also performed across pan-cancer. In addition, the GDSC1 database containing 403 drugs was utilized to explore the relationship between drug sensitivity and G6PD expression levels. Furthermore, we also performed clinical validation and in vitro experiments to further validate the role of G6PD in hepatocellular carcinoma (HCC) cells and its correlation with prognosis. The R software was used for statistical analysis and data visualization.ResultsG6PD expression was upregulated in most cancers compared to their normal counterparts. The study also revealed that G6PD expression was a prognostic indicator and high levels of G6PD expression were correlated with worse clinical prognosis including overall survival, disease-specific survival, and progression-free interval in multiple cancers. Furthermore, the G6PD level was also related to cancer immunity infiltration in most of the cancers, especially in KIRC, LGG, and LIHC. In addition to this, G6PD expression was positively related to pathological stages of KIRP, BRCA, KIRC, and LIHC. Functional analysis and protein-protein interactions network results revealed that G6PD was involved in metabolism-related activities, immune responses, proliferation, and apoptosis. Drug sensitivity analysis showed that IC50 values of most identified anti-cancer drugs were positively correlated with the G6PD expression. Notably, in vitro functional validation showed that G6PD knockdown attenuated the phenotypes of proliferation in HCC.ConclusionG6PD may serve as a potential prognostic biomarker for cancers and may be a potential therapeutic target gene for tumor therapy.
| S-EPMC10435888 | biostudies-literature