A systematic pan-cancer characterization of MEX3A is provided and supports its potential role as a prognostic biomarker and a hypothesis-generating candidate for future mechanistic and clinical validation, as well as suggesting that MEX3A may participate in RNA regulatory networks and tumor-immune microenvironment interactions.
Abstract
MEX3A is an evolutionarily conserved RNA-binding protein characterized by two KH RNA-binding domains and a C-terminal RING domain, suggesting potential roles in both post-transcriptional regulation and protein modification. Although MEX3A has been implicated in several individual cancer types, its shared and cancer-specific roles across human cancers remain incompletely understood. In this study, we performed a comprehensive pan-cancer analysis of MEX3A by integrating publicly available datasets, including TCGA, GTEx, CPTAC, and other external resources. We systematically evaluated MEX3A expression, genetic alterations, phosphorylation status, clinical relevance, RNA modification-related associations, immune-related features, and functional enrichment profiles across multiple tumor types. MEX3A was significantly upregulated in most cancers and showed associations with advanced pathological stage in several tumor types. Survival analyses indicated that elevated MEX3A expression was correlated with poor overall survival and disease-specific survival in cancers such as ACC, LIHC, MESO, and SARC, supporting its potential value as a prognostic biomarker. Genetic alteration analysis revealed frequent copy number amplification of MEX3A in several cancers, whereas these alterations were not consistently associated with survival outcomes. Proteomic analyses further identified altered phosphorylation levels at S338 and S462 in tumor tissues, suggesting that post-translational modification may contribute to the regulation of MEX3A activity in a cancer-type-specific manner. Correlation analyses showed that MEX3A expression was associated with RNA modification-related genes, immune modulators, immune checkpoint genes, tumor-infiltrating immune cells, tumor mutational burden, and microsatellite instability across different cancers. These findings suggest that MEX3A may participate in RNA regulatory networks and tumor-immune microenvironment interactions. Functional enrichment analysis revealed that MEX3A-associated proteins are involved in pathways related to transcriptional dysregulation, mRNA stability, and translational regulation. However, as these findings are primarily based on bioinformatic and correlation-based analyses, they should not be interpreted as evidence that MEX3A is a validated therapeutic or immunotherapy target. Overall, this study provides a systematic pan-cancer characterization of MEX3A and supports its potential role as a prognostic biomarker and a hypothesis-generating candidate for future mechanistic and clinical validation.
An integrated pan-cancer analysis of PABPC1L expression and function in 33 human malignant tumors identified PABPC1L as exhibiting oncogenic properties and is proposed to function as a key regulator of tumorigenesis and immunotherapy resistance.
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Functional enrichment analysis reveals that SLC25A39 is commonly associated with immune-related pathways and cell cycle-related pathways in the pan-cancer dataset.
Li Qin, Yuanqian Yao, Jian-Lin Lv· Discover Oncology· 0 citations
Background WD Repeat Domain 76 (WDR76) plays a potential role in cellular regulation; however, its comprehensive landscape across human malignancies and its specific biological function in hepatocellular carcinoma (HCC) remain largely unexplored. Methods We conducted a systematic pan-cancer analysis utilizing multi-omics data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Cancer Cell Line Encyclopedia (CCLE) atabases to evaluate WDR76 expression, subcellular localization, and its correlation with clinicopathologic features, genomic instability, and immune infiltration. Diagnostic and prognostic values were assessed via Receiver operating characteristic (ROC) and Kaplan-Meier analyses. Furthermore, the functional role of WDR76 in HCC was validated in vitro using Hep-3B and Huh7 cell lines through siRNA-mediated knockdown, followed by CCK-8, wound-healing, and transwell assays. Results WDR76 was significantly upregulated in the majority of tumor types, including LIHC, LUAD, and COAD, while exhibiting nuclear localization. Elevated WDR76 expression correlated with advanced tumor staging, metastasis, and poor clinical outcomes across multiple cohorts, particularly in ACC, KIRP, and LIHC. ROC analysis highlighted its exceptional diagnostic precision in cancers such as GBM and LIHC. Immunologically, WDR76 expression was intricately linked to immune cell infiltration, immune checkpoint markers, and genomic instability parameters, suggesting a role in shaping the tumor microenvironment. Drug sensitivity profiling revealed that high WDR76 levels correlate with resistance to specific chemotherapeutic agents. Experimentally, silencing WDR76 in HCC cells significantly suppressed cell proliferation, migration, and invasion capabilities. Conclusion Our study establishes WDR76 as a robust pan-cancer prognostic biomarker and a potential immunotherapeutic target. Specifically, we provide experimental evidence that WDR76 functions as an oncogenic driver in liver cancer, promoting malignant phenotypes and offering a novel avenue for targeted therapeutic intervention.
Yi-Fan Wang, Rong Zhou, Shen-Long Guo et al.· International Journal of Imm...· 0 citations
Background: Given that aberrant glycosylation acts as a catalyst for tumorigenesis, elucidating Signal Sequence Receptor 2 (SSR2)'s specific patterns is essential to unlock its potential as a prognostic biomarker and clarify its mechanistic role in cancer biology. This study aims to comprehensively characterize the expression landscape and functional significance of SSR2, a pivotal subunit of the oligosaccharyltransferase complex, across normal human tissues and diverse malignancies. Methods: In this investigation, we utilized advanced bioinformatics resources, including the Human Protein Atlas (HPA), Genotype-Tissue Expression (GTEx), The Cancer Genome Atlas (TCGA), and CPTAC databases, to analyze the expression levels of SSR2 across various human tissues and malignancies. The data were analyzed utilizing the Xiantao academic analysis tool. We performed comparative analyses of SSR2 expression in cancerous and adjacent normal tissues, assessed survival outcomes associated with SSR2 expression levels, and conducted mutation and methylation analyses using cBioPortal and other relevant platforms. Results: Our findings revealed that SSR2 was predominantly expressed in the pancreas, epididymis, and ovary. Notably, significant differences in SSR2 expression were observed between cancerous and adjacent normal tissues in bladder urothelial carcinoma, breast cancer, and colorectal cancer. High levels of SSR2 correlated with poorer overall survival in adrenocortical carcinoma, esophageal cancer, and clear cell renal carcinoma, while SSR2 expression exhibited a protective effect in ovarian serous cystadenocarcinoma. Furthermore, SSR2 mutations were frequently observed in uterine sarcoma and liver cancer. Methylation analysis identified cg24557248, a CpG site, as a promising prognostic biomarker in clear cell renal carcinoma; increased methylation at this site was linked to improved survival outcomes. Conclusions: This study emphasizes the complex role of SSR2 in cancer biology, showcasing its potential as both a biomarker and a therapeutic target. Furthermore, the link between SSR2 and tumor immune cell infiltration indicates its role in shaping tumor microenvironments. Future investigations should aim to clarify how SSR2 affects tumor growth and immune regulation, which could lead to innovative therapeutic approaches for cancer treatment.
Integrative analyses and experimental validation suggest that DDX52 is a potential prognostic biomarker and therapeutic target in LIHC and its associations with immune features and multiple cancer-related pathways provide hypotheses for future mechanistic investigation.
Chong-Yu Zhang, Qian-Kun Wang, Mengchen Zhu et al.· Molecular and Cellular Probe...· 0 citations
Collectively, m6A-related genes are dysregulated in breast cancer and correlate with patient outcomes, highlighting their biomarker potential, with YTHDF3 warranting in-depth investigation.
Pu Jin, Yue-Tsz Fan· Journal of Visualized Experi...· 0 citations
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