Background and Objectives: A thorough comprehension of the essential molecules and related processes underlying the carcinogenesis, proliferation, and recurrence of acute myeloid leukemia (AML) is crucial. This study aimed to investigate the expression levels, diagnostic and prognostic significance and biological roles of Bcl-2-associated athanogene 4 (BAG4) in AML carcinogenesis. Materials and Methods: Gene expression profiles were analyzed using publicly available datasets, particularly GSE9476 and TCGA, using tools such as GEO2R, GEPIA2, UALCAN and TIMER2.0. The immune infiltration correlation was examined using the GSCA platform, while the function of BAG4 at the single-cell level was analyzed via CancerSEA. Protein–protein and gene–gene interaction networks were constructed using STRING and GeneMANIA, and enrichment analyses were performed using GO, KEGG and DAVID. Expression validation was performed using RT-qPCR in HL-60 (AML) and HaCaT (normal) cells, and ROC curve analysis evaluated the diagnostic accuracy. Results: BAG4 was significantly overexpressed in AML tissues and cell lines compared with healthy controls. High BAG4 expression was associated with poor overall survival and strong diagnostic power (AUC = 0.944). BAG4 was positively associated with immune cell infiltration and negatively associated with CD4+/CD8+ T and NK cells. At the single-cell level, BAG4 was associated with proliferation, invasion, and DNA repair functions. Functional network analysis showed that BAG4 interacted with apoptosis and necroptosis-related genes such as BCL2, BAG3 and TNFRSF1A and was enriched in pathways such as NF-κB, TNF signaling and apoptosis. Conclusions: BAG4 is overexpressed in AML and is associated with adverse clinical outcomes and immune modulation. It may play an important role in leukemogenesis by affecting apoptotic resistance and immune evasion. BAG4 has potential as a diagnostic biomarker and treatment target in AML, but further in vivo and clinical validation is needed.

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by uncontrolled proliferation of myeloid cells. MicroRNAs (miRNAs), small noncoding RNAs, regulate post-transcriptional gene expression by degrading target mRNAs or repressing translation. Dysregulated miRNA expression has been implicated in various malignancies, including CML, where they can function as oncogenes or tumor suppressors. This study aimed to investigate the relationship between miR-122-5p and cell division cycle 25A (CDC25A) in CML and to elucidate the regulatory mechanisms of miR-122-5p. This study integrates bioinformatics analysis with in vitro RT-qPCR validation in K562 chronic myeloid leukemia cells to explore the potential regulatory relationship between miR-122-5p and CDC25A. mRNA expression profiles were retrieved from the GSE100026 dataset in the Gene Expression Omnibus (GEO), and differentially expressed genes were identified using GEO2R. Quantitative real-time PCR (RT-qPCR) was performed to measure miR-122-5p, CDC25A, and cyclin-dependent kinase 4 (CDK4) expression levels. Bioinformatics analyses (miRNeT, miRDIP, TargetScan, BioGPS, GeneMANIA, STRING) were applied to predict molecular interactions and functional pathways. Public RNA-seq datasets and in silico tools were used to prioritize candidates; RT-qPCR in a single CML cell line (K562) provided in vitro expression validation. In K562 cells, miR-122-5p expression was significantly reduced, while CDC25A and CDK4 were markedly upregulated. Bioinformatics tools confirmed CDC25A as a potential miR-122-5p target. Functional enrichment indicated CDC25A involvement in cell cycle regulation and apoptosis. These findings suggest that miR-122-5p functions as a tumor suppressor in CML by targeting CDC25A. Modulating the miR-122-5p/CDC25A axis may provide potential molecular targets for inhibiting CML progression through regulation of cell cycle pathways. Findings are exploratory and based on bioinformatics with limited in vitro expression confirmation; functional studies are required to establish causality.

Gastrointestinal tract cancers account for approximately one-third of cancer-related deaths. Early diagnosis and effective treatment are the most important ways to prevent cancer-related morbidity and mortality. ROMO1 has been shown to play an important role in many types of cancer. However, the biological function of ROMO1 is still poorly understood in gastrointestinal system cancers. The aim of this study is to reveal the expression change and oncogenic role of ROMO in gastrointestinal system cancers. Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN, TIMER, GeneMANIA, TISIDB, and STRING were applied to assess the biological function of ROMO1 in gastrointestinal cancers (colon adenocarcinoma (COAD), esophageal carcinoma (ESCA), liver hepatocellular carcinoma (LIHC), pancreatic adenocarcinoma (PAAD), and stomach adenocarcinoma (STAD)). ROMO1 is significantly increased in COAD, ESCA, LUHC, and PAAD, and the overexpression of ROMO1 is associated with clinicopathological features. In addition, ROMO1 has been found to be closely associated with tumor-infiltrating immune cells in gastrointestinal cancers. ROMO1 is closely related to the inner mitochondrial membrane proteins (TIMM) family. The study revealed that ROMO1 is of significant clinical importance for gastrointestinal cancers and may have potential clinical utility in treatment and prognosis. Functional tests on cell lines derived from these particular gastrointestinal cancers can also be performed in vitro to evaluate the impact of the ROMO1 gene and other factors, like potential drugs, on the expression of these genes and the development and progression of the cancer.

Background/Objectives: Metabolic syndrome (MetS) is a complex clinical condition characterized by the coexistence of interrelated metabolic abnormalities that significantly increase the risk of cardiovascular diseases and type 2 diabetes mellitus. Endocan, an endothelial cell-specific molecule, is considered a biomarker of endothelial dysfunction and inflammation. This study aimed to evaluate the relationship between serum endocan levels and the severity of MetS, assessed using the MetS-Z score. Methods: In this study, 120 patients with MetS and 50 healthy controls were included. MetS was diagnosed according to the NCEP-ATP III criteria. The MetS-Z scores were calculated using the "MetS Severity Calculator" (https://metscalc.org). Serum levels of Endocan, sICAM-1, and sVCAM-1 were measured by ELISA method. Results: Serum levels of endocan, sICAM-1, and sVCAM-1 were significantly higher in the MetS group compared to the control group (all p< 0.001). When the MetS group was divided into tertiles based on MetS-Z scores, a stepwise and statistically significant increase was observed in the levels of endocan and other endothelial markers from the lowest to the highest tertile (p< 0.0001). Correlation analysis revealed a strong positive association between the MetS-Z score and serum endocan levels (r=0.584, p< 0.0001). ROC curve analysis showed that endocan had high diagnostic accuracy for identifying MetS (AUC=0.967, p< 0.0001), with a cutoff value of >88.0 ng/L. Conclusion: Circulating levels of Endocan were significantly increased in MetS and also were associated with the severity of MetS, suggesting that the levels of endocan may be a potential role of the cellular response to endothelial dysfunction injury in patients with MetS.