Pan-cancer analysis of the prognostic value of C12orf75 based on data mining.
Ontology highlight
ABSTRACT:
SUBMITTER: Cai G
PROVIDER: S-EPMC8221310 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:BackgroundAs a member of the exon junction complex (EJC), RNA-binding motif protein 8A (RBM8A) plays a crucial role in the maintenance of mRNA and multiple activities of an organism. Immunotherapy has been proven to be a staple type of cancer treatment. However, the role of RBM8A and immunity across cancer types is unclear.ObjectiveThis study aims to visualize the expression, prognosis, mutations, and coexpressed gene results of RBM8A across cancer types and to explore the link between RBM8A expression and immunity.MethodsIn this study, data were collected from multiple online databases. We analyzed the data using the HPA, UALCAN Database, COSMIC, cBioPortal, Cancer Regulome tools, Kaplan-Meier Plotter, and TIMER website.ResultsFor the expression of RBM8A in normal tissues, higher expression of RBM8A was observed in immune-related cells than in nonimmune organs. The expression level of RBM8A was related to tumor type. Missense mutations in RBM8A were found in most tumors and affected the prognosis of carcinomas with coexpressed genes. RBM8A was strongly associated with immune-infiltrating cells and immune checkpoint inhibitors, especially in LIHC.ConclusionsRBM8A is a gene worth exploring and may be a unique immune target in the future.
| S-EPMC8277506 | biostudies-literature
Project description:Objective: APBB1IP is a Rap1-binding protein that mainly acts as a regulator of leukocyte recruitment and pathogen clearance through complement-mediated phagocytosis. However, the role of APBB1IP in tumor immunity remains unclear. This study was carried out to evaluate the prognostic landscape of APBB1IP in pan-cancer analysis and investigate the relationship between APBB1IP expression and immune infiltration. Methods: We explored the expression pattern and prognostic value of APBB1IP in pan-cancer analysis through Kaplan-Meier Plotter and multiple databases, including TCGA, Oncomine. We then assessed the correlation between APBB1IP expression and immune cell infiltration using the TIMER database. Furthermore, we identified the proteins that interact with APBB1IP and performed epigenetic and transcriptional analyses. Multivariate Cox regression analyses were applied to construct a prognostic model, which consisted of APBB1IP and its interacting proteins, based on the lung cancer cohorts from the Gene Expression Omnibus (GEO) database. Results: The expression of APBB1IP was correlated with the prognosis of several types of cancer. APBB1IP upregulation was found to be associated with increased immune cell infiltration, especially for CD8+ T cells, natural killer (NK) cells, and immune regulators. A link was found between APBB1IP and immune-related proteins including RAP1A/B, TLN1/2 and VCL in the interaction network. Conclusion: APBB1IP can serve as a prognostic biomarker in pan-cancer analysis. APBB1IP upregulation was correlated with increased immune-cell infiltration, and the expression APBB1IP in different tumors might be related to the tumor immune microenvironment.
| S-EPMC7738982 | biostudies-literature
Project description:Microtubule-interacting and trafficking domain containing 1 (MITD1) is associated with abscission during cytokinesis. However, systematic investigation into its role in cancer is lacking. Therefore, we explored the pan-cancer role of MITD1 using multiple databases. Expression and clinical survival, immunological, and enrichment analyses were performed using R packages and online tools. For breast cancer, single-cell level analysis, immunochemistry, and in vitro experiments were performed to explore the mechanism of MITD1. A nomogram was established to predict the prognosis of patients with breast cancer and evaluate the immunotherapy biomarker based on two datasets. In some cancers, high MITD1 expression was associated with a more favorable prognosis. For instance, it inhibited tumor cell proliferation and migration in breast cancer. MITD1 may regulate cancer development by altering the tumor microenvironment, and MITD1 expression may predict the response to immune checkpoint blockade, platinum, and poly ADP-ribose polymerase inhibitor therapies. Our nomogram was used to determine the prognosis of patients with breast cancer. MITD1 can also predict the response to immunotherapy. Our first pan-cancer study of MITD1 has shown that it plays different roles in cancer development and therapy. In breast cancer, MITD1 inhibited cell proliferation and migration and serves as a new biomarker.
| S-EPMC9600621 | biostudies-literature
Project description:Colon cancer is one of the top five cancers with the highest incidence rate in the world. In order to better understand the pathogenesis and progression of colon cancer, it is still necessary to investigate the abnormally expressed genes in cancer tissue. In this study, the Oncomine database was used for expression analysis, and it was found that the expression level of gamma-aminobutyric acid type A receptor subunit delta (GABRD) gene was upregulated in colon cancer tissue compared with that in normal tissue. UALCAN was used to analyze the expression of GABRD in different groups of age, gender, cancer stage, N stage, and histological subtype. Then, it was also found that the expression of GABRD in each subgroup of colon cancer tissue was all high compared with that in normal tissue. LinkedOmics was used to screen out the differentially expressed genes related to GABRD expression in colon cancer. GO annotation and KEGG pathway enrichment analyses found that the correlated genes may be related to breast cancer, human papillomavirus infection, Notch signaling pathway, and other pathways. Thereafter, GSEA was performed to obtain GABRD-related kinases, miRNAs, and transcription factors, and gene interaction networks were constructed. It was found that GABRD may be involved in cell cycle regulation. Finally, websites like GEPIA were used to detect the predictive ability of GABRD on the prognosis of patients with colon cancer. Kaplan-Meier analysis suggested that the upregulation of GABRD expression was related to the poor prognosis of patients with colon cancer. Overall, in this study, the potential role and prognostic ability of GABRD in colon cancer were explored through data mining, which can be a clue for further research on GABRD.
| S-EPMC8203377 | biostudies-literature
Project description:Heat shock factor 2 (HSF2), a transcription factor, plays significant roles in corticogenesis and spermatogenesis by regulating various target genes and signaling pathways. However, its expression, clinical significance and correlation with tumor-infiltrating immune cells across cancers have rarely been explored. In the present study, we comprehensively investigated the expression dysregulation and prognostic significance of HSF2, and the relationship with clinicopathological parameters and immune infiltration across cancers. The mRNA expression status of HSF2 was analyzed by TCGA, GTEx, and CCLE. Kaplan-Meier analysis and Cox regression were applied to explore the prognostic significance of HSF2 in different cancers. The relationship between HSF2 expression and DNA methylation, immune infiltration of different immune cells, immune checkpoints, tumor mutation burden (TMB), and microsatellite instability (MSI) were analyzed using data directly from the TCGA database. HSF2 expression was dysregulated in the human pan-cancer dataset. High expression of HSF2 was associated with poor overall survival (OS) in BRCA, KIRP, LIHC, and MESO but correlated with favorable OS in LAML, KIRC, and PAAD. The results of Cox regression and nomogram analyses revealed that HSF2 was an independent factor for KIRP, ACC, and LIHC prognosis. GO, KEGG, and GSEA results indicated that HSF2 was involved in various oncogenesis- and immunity-related signaling pathways. HSF2 expression was associated with TMB in 9 cancer types and associated with MSI in 5 cancer types, while there was a correlation between HSF2 expression and DNA methylation in 27 types of cancer. Additionally, HSF2 expression was correlated with immune cell infiltration, immune checkpoint genes, and the tumor immune microenvironment in various cancers, indicating that HSF2 could be a potential therapeutic target for immunotherapy. Our findings revealed the important roles of HSF2 across different cancer types.
| S-EPMC8787226 | biostudies-literature
Project description:Endoplasmic reticulum (ER) stress-related genes are closely related to the occurrence, development, and immunotherapy response of tumors. This study provides a comprehensive assessment of HSPA5 from a pan-cancer perspective using multi-omics data. We analyzed the function of HSPA5 in multiple tumor types using multiple databases. Finally, immunohistochemistry was used to examine the relationship between HSPA5 expression in tissue microarrays from 100 patients with bladder cancer and the prognosis of patients with bladder cancer. Using the TCGA database, we were able to determine that HSPA5 is significantly elevated in a number of common malignancies and is linked with a bad prognosis. Cox regression analysis showed that the high expression of HSPA5 was correlated with OS, progression free survival (PFS), disease free survival (DFS), and disease special survival (DSS) of adrenocortical carcinoma (ACC). In addition, we discovered significant disparities in HSPA5 methylation and phosphorylation levels between various malignancies and normal tissues. HSPA5 expression was significantly correlated with the levels of infiltrating cells and immune checkpoint genes. HSPA5 is highly expressed in bladder cancer and patients with high HSPA5 expression have a poor prognosis. Our study provides a basis for further understanding of the role of ER stress-related gene HSPA5 in different tumor genesis and development. HSPA5 has also been shown to be a prognostic biomarker for bladder cancer patients.
| S-EPMC10944199 | biostudies-literature
Project description:Background and aims:This study aimed to clarify the prognostic role of LINC01296 in various cancers, and to evaluate its effect on proliferation, metastasis, and the cell cycle in hepatocellular carcinoma (HCC) by data mining, bioinformatics, and in vitro validation. Methods:The prognostic role of LINC01296 in cancer patients was assessed by searching the PubMed, Embase, Web of Science, and Gene Expression Omnibus databases and calculating pooled hazard ratios (HRs) with 95% confidence intervals (CIs); this prognostic role was also evaluated using The Cancer Genome Atlas (TCGA). We detected LINC01296 expression in HCC cell lines, and lentivirus-mediated small interfering RNAs were used to silence LINC01296 in MHCC97H and Hep3B cells to explore the role of LINC01296 in cell proliferation, metastasis, and cell cycle progression with in vitro validation and bioinformatics. Results:The results indicated that LINC01296 overexpression was associated with poor overall survival (OS) and disease-free survival (DFS) in various cancers; however, LINC01296 expression was not associated with recurrence-free survival (RFS). Similar results were found with TCGA, which showed that LINC01296 expression was associated with the pathologic stage, tumor size, and differentiation in Asian cancer patients. Additionally, bioinformatics analysis revealed expression of 394 related genes, which indicated that LINC01296 could be involved in the tumorigenesis and progression of HCC. In vitro gene silencing experiments indicated that LINC01296 downregulation repressed cell proliferation, cell cycle progression, and the metastatic potential of HCC through the regulation of BUB1, CCNA2, and CDK1 expression. Conclusion:This study demonstrated that LINC01296 expression is related to poor OS and DFS in a variety of cancer types and that LINC01296 has an oncogenic role in HCC.
| S-EPMC6650622 | biostudies-literature
Project description:The occurrence of cancer is closely related to the deregulation of certain pathways. Based on pathway deregulation scores (PDS) inferred by the Pathifier algorithm, we analyzed transcriptomic data of 13 different cancer types in The Cancer Genome Atlas database to identify cancer-specific deregulated pathways and prognostic pathways. The results showed that the individual-specific pathway deregulation scores can clearly distinguish different cancer types and their tumor-adjacent tissues. In addition, the cancer-specific deregulated pathways and prognostic pathways of different cancer types had high heterogeneity, and the identified cancer prognostic pathways have been reported to be closely related to the corresponding cancers. Furthermore, we also found that cancers with more deregulation pathways tend to be malignant and have worse prognoses. Finally, a Cox proportional Hazards model was constructed based on the prognostic pathways; this model successfully predicted survival and prognosis based on data from cancer samples. In addition, the performance of the breast cancer prognostic model was validated with an independent data set in the METABRIC database. Therefore, the prognostic pathways we identified have the potential to become targets for the treatment of cancer.
| S-EPMC8615289 | biostudies-literature
Project description:IntroductionKLRB1 is a gene encoding CD161 expressed in NK cells and some T cell subsets. At present, KLRB1 is believed to affect tumorigenesis and development by regulating the cytotoxicity of NK cells in several cancers. However, there is a lack of systematic reviews of KLRB1 in a variety of malignancies.ObjectivesHence, our research is aimed at providing a relatively comprehensive understanding of the role of KLRB1 in different types of cancer, paving the way for further research on the molecular mechanism and immunotherapy potential of KLRB1.MethodsIn this study, we used relevant public databases, including TCGA (The Cancer Genome Atlas), GEO (Gene Expression Omnibus), CCLE (Cancer Cell Line Encyclopedia), GTEx (Genotype Tissue-Expression), and HPA (Human Protein Atlas), to perform a pan-cancer analysis of KLRB1 across 33 types of cancer. We explored the potential molecular mechanism of KLRB1 in clinical prognosis and tumor immunity from the aspects of gene expression, survival status, clinical phenotype, immune infiltration, immunotherapy response, and chemotherapeutic drug sensitivity.ResultsKLRB1 was downregulated in 13 cancers while upregulated in kidney cancer. Patients with high expression of KLRB1 have a better prognosis in most types of cancer. Moreover, the KLRB1 expression level is related to TMB and MSI and related to various immune signatures of tumor. The expression of KLRB1 can affect tumor immune cell infiltration. KLRB1 expression level can also affect the sensitivity of chemotherapy drugs.ConclusionsKLRB1 may be a prognostic and immunological biomarker across tumors. At the same time, KLRB1 expression can reflect the sensitivity of cancer patients to chemotherapy drugs. KLRB1 may become a new target for immunotherapy.
| S-EPMC8749375 | biostudies-literature
Project description:BackgroundOsteomimicry of cancer cells had been widely reported in prostate cancer and breast cancer. However, the prognostic value of osteomimicry in various cancer types remained unclear. We hypothesized that osteomimicry would result in remodeling of the tumor microenvironment and was eligible to predict patient prognosis.MethodsA comprehensive transcriptomic analysis of the osteomimicry, which was characterized by mRNA expression of SPARC, SPP1, and BGLAP, across 20 solid tumors (7564 patients) using RNA-seq data from The Cancer Genome Atlas (TCGA) was conducted. Samples of each cancer type were classified into subgroups (high vs. low) based on median value of osteomimetic markers, the associations of these markers with clinical outcomes, immune cell infiltration and immune checkpoints expression were explored.ResultsEach osteomimetic marker harbored prognostic value in the pan-cancer analyses [SPARC: hazard ratio (HR) = 1.10, p = 0.028; SPP1: HR = 1.25, p < 0.001; BGLAP: HR = 1.13, p = 0.005]. Patients with high expression of all the three genes also had significantly unfavorable survival (HR = 1.61, p < 0.0001) compared with those of low expression. Correlation analyses demonstrated that osteomimicry was closely related to tumor purity, dendritic cells (DC) infiltration and expression of immune checkpoints.ConclusionOsteomimicry had prognostic value in various cancer types and the underlying mechanism might correlate to the trapping and dysfunction of DCs in the tumor microenvironment, revealing the potential of osteomimicry as a target of immunotherapy.
| S-EPMC7678014 | biostudies-literature