Epigenetic changes regulate gene expression through histone modifications, chromatin remodeling, and protein translation of these modifications. The PRC1 and PRC2 complexes shape gene repression via histone modifications. Specifically, the CBX protein family aids PRC1 recruitment to chromatin, impacting the progressive multistep process driving chromatin silencing. Among family members, CBX3 is a complex protein involved in aberrant epigenetic mechanisms that drive lung cancer progression. CBX3 promotes lung tumorigenesis by interacting with key pathways such as PI3K/AKT, Ras/KRAS, Wnt/β-catenin, MAPK, Notch, and p53, leading to increased proliferation, inhibition of apoptosis, and enhanced resistance to therapy. Given our current lack of knowledge, additional research is required to uncover the intricate mechanisms underlying CBX3 activity, as well as its involvement in molecular pathways and its potential biomarker evaluation. Specifically, the dissimilar roles of CBX3 could be reexamined to gain a greater insight into lung cancer pathogenesis. This review aims to provide a clear overview of the context-related molecular profile of CBX3, which could be useful for addressing clinical challenges and developing novel targeted therapies based on personalized medicine.

Infective endocarditis (IE) arises from complex interactions between microbial pathogens and host hemostasis systems, where dysregulated coagulation mediates microbial persistence and systemic thromboembolic complications. Alterations in primary, secondary, and tertiary hemostasis in the acute IE phase have direct clinical implications for vegetation formation and detachment. Staphylococcus aureus is one of the most common pathogens that causes IE, and it is capable of profoundly altering the coagulation cascade through several mechanisms, such as platelet activation, prothrombin activation through staphylocoagulase release, and plasminogen stimulation via staphylokinase production. Understanding these complex and yet unmasked mechanisms is of pivotal importance to promoting targeted therapeutic intervention aimed at reducing IE morbidity and mortality. Moreover, the management of antiplatelet and anticoagulant treatment during IE onset is a controversial issue and needs to be tailored to patient comorbidities and IE-related complications, such as cerebral embolism. This review provides a roadmap to promote clinicians’ understanding of the complex interactions between hemostasis and IE clinical manifestations and complications, discussing pathogen-specific coagulation profiles while addressing critical knowledge gaps for IE management.

Background and Objective Colorectal cancer remains a major global health challenge, necessitating the development of accurate non-invasive diagnostic tools. Circulating and excretory microRNAs (miRNAs) are promising biomarkers owing to their stability and regulatory roles in tumorigenic pathways. While single miRNA assays often lack sufficient diagnostic accuracy, panels combining multiple miRNAs have shown enhanced performance. This systematic review and meta-analysis evaluated the diagnostic accuracy of multi-miRNA panels and explored their mechanistic relevance to colorectal cancer pathogenesis. Methods A comprehensive search of PubMed, Embase, Web of Science, and Scopus was conducted through March 2025 following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The study protocol was registered with PROSPERO (CRD420251060655). Eligible studies assessed the diagnostic accuracy of multi-miRNA panels for colorectal cancer using extractable data on sensitivity, specificity, and area under the curve. Data were extracted independently by two reviewers. A bivariate random-effects model was used to calculate pooled diagnostic estimates. Study quality was assessed with the Quality Assessment of Diagnostic Accuracy Studies 2 (QUADAS-2) tool, and heterogeneity was evaluated using I² statistics. Subgroup analyses were conducted by sample type (e.g., plasma, serum, stool) and panel size. Target genes of recurrent miRNAs were mapped to canonical colorectal cancer-related pathways. Results Twenty-nine studies comprising 5497 participants (3070 colorectal cancer cases and 2427 controls) and 35 multi-miRNA panels were included. Pooled sensitivity was 0.85 (95% confidence interval 0.80–0.88), specificity was 0.84 (95% confidence interval 0.80–0.88), and the area under the curve was 0.90, despite substantial heterogeneity (I² > 77%). Panels derived from plasma samples showed the highest balanced performance (sensitivity 0.88; specificity 0.87), while three-miRNA panels exhibited the best diagnostic trade-offs. Mechanistic analysis of 42 recurrent miRNAs revealed consistent involvement in key colorectal cancer pathways, including PI3K/AKT, Wnt/β-catenin, epithelial-mesenchymal transition, angiogenesis, and immune regulation. Conclusions Multi-miRNA panels derived from diverse biospecimen sources demonstrate high diagnostic accuracy for colorectal cancer and are mechanistically linked to fundamental oncogenic pathways. Future efforts should focus on panel standardization, biospecimen-specific validation, and integration into clinical workflows to advance precision oncology.

Epigenetic changes regulate gene expression through histone modifications, chromatin remod-eling and proteins interpreter of these modifications. The PRC1 and PRC2 complexes shape gene repression via histone modifications. Specifically, the CBX protein family aids PRC1 recruitment to chromatin, impacting the progressive multistep process driving chromatin silencing. Among family members, CBX3 is a complex protein involved in aberrant epigenetic mechanisms that drive lung cancer progression. CBX3 promotes lung tumorigenesis by interacting with key pathways such as PI3K/AKT, Ras/KRAS, Wnt/β-catenin, MAPK, Notch, and p53, leading to in-creased proliferation, inhibition of apoptosis, and enhanced resistance to therapy. Given our current lack of knowledge, additional research is required to uncover the intricate mechanisms underlying CBX3 activity, as well as its involvement in molecular pathways and its potential biomarker evaluation. Specifically, the dissimilar roles of CBX3 could be reexamined in order to gain a greater insight into lung cancer pathogenesis. This review aims to provide a clear overview of the context-related molecular profile of CBX3, which could be useful for addressing clinical challenges and developing novel targeted therapies based on personalized medicine.

Cardiovascular disease (CVD) is the primary cause of mortality globally with a multifactorial etiology that involves epigenetics. Chromobox 3 (CBX3), the major isoform of heterochromatin protein 1, is involved in intricate epigenetic mechanisms affecting congestive heart failure. In patients with CVD affected by lung cancer risk, CBX3 exerts a sophisticated mechanism of action, suppressing the proliferation, migration, and formation of neointima in vascular smooth muscle cells (VSMCs) by affecting the Notch3 pathway, indicating a potential protective function against vascular remodeling and atherosclerosis. However, the broader impact of CBX3 on endothelial function, as well as its effects on monocyte/macrophage and lymphocyte infiltration and function within the arterial wall, remain poorly understood. Since very little is known so far, more definite research would be needed to reveal the fine mechanisms of CBX3 action, along with its relationship in molecular processes and prospects as a biomarker. Specifically, CBX3 biological features could be examined to gain a greater insight into CVD risks. This review outlines the role of CBX3 in mechanisms associated with CVD and feasibility for optimizing pre-existing therapy and developing new therapeutic strategies based on personalized medi-cine.