S. M. Abdus Salam

The survival rate of patients with advanced laryngeal cancer has not substantially improved over time. RNA sequencing analysis identified Keratin-1 (KRT1) as a gene potentially associated with cancer recurrence. This study investigated the association between KRT1 expression and recurrence in advanced laryngeal cancer. RNA sequencing was performed to identify candidate genes associated with recurrence. The effects of KRT1 expression on clinical outcomes were evaluated in patients with laryngeal cancer. Multiple experimental techniques were utilized. RNA sequencing of patient samples demonstrated higher KRT1 gene expression in the recurrence group than in non-recurrent cases. Patients with KRT1-positive immunostaining exhibited trends of worse overall survival (OS) and recurrence-free survival (RFS). In vitro studies showed that KRT1 knockdown suppressed tumor cell invasion, cell migration, and expression of epithelial–mesenchymal transition (EMT)-related genes in human head and neck squamous cell carcinoma (HNSCC) cell lines. KRT1 knockdown enhanced tumor cell apoptosis and exhibited synergistic effects with conventional radiation and chemotherapy treatments. KRT1 may serve as a biomarker for predicting advanced laryngeal cancer recurrence and assist with selecting patients to receive concurrent chemoradiotherapy (CCRT). Further molecular investigations are warranted to determine its effects, but KRT1 has potential as a therapeutic target.

Background: Glioblastoma multiforme (GBM) represents one of the most aggressive and lethal primary brain malignancies, characterized by rapid proliferation, extensive invasiveness, and a dismal prognosis. Emerging evidence implicates nucleotide-binding oligomerization domain-containing protein 2 (NOD2), an intracellular pattern recognition receptor, as a potential driver of GBM progression. This study investigates NOD2’s role in promoting glioblastoma through its effects on the epithelial–mesenchymal transition (EMT) and cancer stem cell (CSC) markers. Methods: NOD2 expression levels and survival outcomes were assessed using TCGA data from GBM tumor samples (n = 153) and normal brain tissues (n = 5). NOD2 protein expression was validated in glioma cell lines using Western blot and immunofluorescence analyses. Functional studies employed siRNA-mediated NOD2 knockdown to evaluate effects on cellular proliferation, migration, invasion, and colony formation, while correlations between NOD2 and EMT/CSC markers were assessed. Results: The analysis of TCGA data revealed a significantly elevated NOD2 expression in GBM tumors compared to normal brain tissue, with a high NOD2 expression correlating with a reduced disease-free survival in GBM patients. All tested glioma cell lines demonstrated robust NOD2 expression. Functional analyses demonstrated that NOD2 depletion substantially impaired cellular proliferation, migration, invasion, and the colony-forming capacity. Mechanistically, siRNA-mediated NOD2 knockdown significantly decreased the expression of EMT (Snail, SLUG, Vimentin) and CSC markers (CD44, CD133) at both protein and mRNA levels. Conclusions: Our results indicate that NOD2 contributes to GBM progression by influencing EMT and CSC pathways. These findings suggest NOD2’s potential as a therapeutic target in glioblastoma, highlighting the need for further mechanistic studies and therapeutic exploration.

Purpose Cardiovascular diseases (CVDs) continue to be the leading cause of death globally, driven by a complex interplay of genetic, epigenetic, and environmental factors. Traditional risk factors alone fail to explain the individual variability in disease susceptibility and progression. Recent advances in genomics and epigenomics have revealed key molecular mechanisms that regulate cardiovascular function, highlighting the importance of gene network dynamics and epigenetic regulation. Methods This review systematically analyzes peer-reviewed literature from the past decade sourced from electronic databases including PubMed and Google Scholar. It compiles the multifaceted roles of DNA methylation, histone modifications, chromatin remodeling, and noncoding RNAs in regulating cardiovascular gene expression, cellular phenotypes, and disease pathogenesis. Results DNA methylation influences the transcriptional activity of gene expression associated with atherosclerosis, myocardial infarction, and hypertension, while histone modifications and ATP-dependent chromatin remodeling regulate cardiac hypertrophy, fibrosis, and regeneration. Noncoding RNAs further act as critical regulators of angiogenesis, inflammation, and myocardial remodeling. Therapeutically, these findings have facilitated the development of epigenetic drugs and gene-editing technologies targeting specific molecular pathways involved in CVD progression. Emerging technologies such as CRISPR/Cas9, RNA-based therapies, and small-molecule inhibitors of epigenetic enzymes hold potential for correct abnormal gene expression patterns. Moreover, integrative multi-omics and systems biology approaches are advancing personalized treatment strategies, improving the accuracy and effectiveness of cardiovascular interventions. Conclusion Collectively, unraveling the complex molecular interactions among gene networks, epigenetic alterations, and targeted therapeutic mapping aims to combat CVD with better precision and efficacy. Graphical Abstract