Search Results (8,850)

Biological aerosols represent a significant challenge for modern CBRN defense due to their potential for long-range dispersion and the need for rapid threat assessment. Current stand-off detection systems are effective in recognizing anomalous aerosol clouds but often lack the molecular specificity required for reliable agent identification. This review examines the role of mid-infrared (MIR) spectroscopy as an emerging approach for chemically resolved stand-off bioaerosol sensing. The physical principles of MIR detection are discussed, including molecular vibrational fingerprints, differential scattering (DISC), and circular intensity differential scattering (CIDS), together with their relationship to aerosol optical properties and Mie resonance effects. Existing and emerging sensing architectures are reviewed, ranging from operational CO₂ laser-based DISC systems to semiconductor-based platforms utilizing tunable differential absorption lidar (DIAL), Quantum Cascade Lasers (QCLs), and dual-comb spectroscopy. The analysis highlights the ability of MIR sensing to access biomolecular signatures associated with proteins, lipids, nucleic acids, and bacterial spores, while also addressing challenges related to atmospheric attenuation, biological variability, and signal interpretation. The reviewed literature indicates that MIR spectroscopy offers a promising pathway toward improved stand-off identification of hazardous bioaerosols, supporting early threat detection and enhanced situational awareness in applications including CBRN defense, critical infrastructure protection, environmental monitoring, public health surveillance, and emergency response. Full article

Inflammation is essential for host defense, but, when dysregulated, it contributes to tissue damage and chronic disease. MicroRNA-146a (miR-146a) is a well-recognized negative regulator of inflammatory signaling, primarily through suppression of the NF-κB pathway; however, its broader proteomic impact under inflammatory conditions remains incompletely defined. In this study, we overexpressed an miR-146a mimic in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and applied quantitative mass spectrometry to characterize global protein abundance changes. Functional overexpression was supported by reduced mRNA abundance of the established miR-146a targets TRAF6 and IRAK1 under LPS-stimulated conditions. Proteomic analysis identified 1232 proteins showing differential abundance under the predefined exploratory criteria, including proteins related to NF-κB activity, inflammasome components, nitric oxide synthesis, and IL-6-associated pathways. Proteins linked to interferon-related signaling were also altered. Targeted validation by quantitative RT-PCR and parallel reaction monitoring supported changes in selected inflammatory mediators, including PTGS2, NOS2, MAPKAPK2, and IRF3. Functionally, miR-146a overexpression was associated with reduced LPS-induced nitric oxide and IL-6 production. Together, these findings provide an exploratory proteomic overview of pathways associated with miR-146a overexpression in activated macrophages and suggest that miR-146a is associated with modulation of multiple inflammatory signaling networks under inflammatory conditions. Full article

Background/Objectives: Rhabdomyosarcoma (RMS), the most common pediatric soft tissue sarcoma, includes two main subtypes, embryonal (eRMS) and alveolar (aRMS), each with distinct molecular and clinical characteristics. Although cellular processes underlying RMS and differences between PAX3-FOXO1 fusion-positive and fusion-negative tumors are well known, the contribution of long noncoding RNAs (lncRNAs) remains poorly understood. Methods: Here, we reannotated publicly available microarray datasets to comprehensively profile lncRNA expression and reconstruct lncRNA–miRNA–mRNA regulatory networks in RMS. Results: We identified several lncRNAs with subtype-specific differential expression, including HOTAIR as a potential sponge for miR-206, DSCR8 for miR-885-5p, and PRKCQ-AS1 for miR-515-5p in eRMS. Database-supported interaction analyses identified putative regulatory relationships between these lncRNAs and cancer-related miRNAs and mRNAs. Validation using the St. Jude Cloud PeCan platform confirmed distinct lncRNA expression signatures across RMS subtypes and other pediatric solid tumors, supporting subtype-specific regulation. Conclusions: Our findings provide an updated characterization of the lncRNA landscape in RMS and identify candidate lncRNA–miRNA–mRNA regulatory networks that may contribute to disease biology. The proposed regulatory interactions are hypothesis-generating and require experimental validation. Overall, our findings provide a resource for future functional studies and support the investigation of lncRNAs as potential biomarkers and therapeutic targets in RMS. Full article

LncRNA NR_003508 has been implicated in lipopolysaccharide (LPS)-induced acute respiratory distress syndrome. Yet, the involvement of LncRNA NR_003508 in Pseudomonas aeruginosa (PA)-induced autophagy remains elusive. This study aims to reveal the underlying mechanisms of LncRNA NR_003508 in PA-induced autophagy, thereby enhancing the basic research content of the pathogenesis of PA infection. Fluorescence in situ hybridization (FISH) probes and q-PCR revealed that PA infection induced macrophage autophagy accompanied by increasing LncRNA NR_003508, suggesting that LncRNA NR_003508 may participate in competing endogenous RNA (ceRNA)-mediated regulatory networks. Concurrently, autophagic clearance of PA requires LncRNA NR_003508. Then, we used the Gene Expression Omnibus (GEO) database to find that LC3 was considered a core protein in PA-infected autophagy. Furthermore, LncRNA NR_003508 promoted the formation of autophagosomes, which played a positive role in PA clearance. Functionally, bioinformatics analysis and luciferase reporter assays demonstrated that LncRNA NR_003508 promotes the conversion of LC3I to LC3II by sponging miR-344i and facilitates p62 degradation by binding to miR-344g-5p. Taken together, our data established that LncRNA NR_003508 enhanced the formation of autophagosomes induced by PA infection via the miR-344i/LC3 and miR-344g-5p/p62 axes, partly boosting the clearance of PA and providing a theoretical basis and experimental support for understanding the mechanisms underlying PA infection. Full article

Introduction: Bronchopulmonary dysplasia (BPD) remains the most significant complication of extreme prematurity, affecting long-term respiratory outcomes. Because current diagnostic criteria identify only established lesions at 36 weeks postmenstrual age, early non-invasive biomarkers are needed. This pilot study aimed to identify a candidate salivary miRNA panel associated with BPD risk and to explore its pathogenetic relevance through in silico analysis. Methods: Saliva was collected from 20 preterm infants (10 with BPD and 10 controls), and miRNA expression was profiled using the GeneChip™ miRNA 4.1 Array Plate. Discriminatory performance was explored by ROC analysis within this discovery cohort, together with power and Spearman correlation analyses. Results: Expression of hsa-let-7b-5p, hsa-let-7c-5p, and hsa-miR-4454 was significantly elevated in the BPD group (p < 0.05, log₂FC ≥ 1.0), with no significant correlation with gestational age or birth weight. Bootstrap-corrected AUC values ranged from 0.905 to 0.937 and were supported by leave-one-out cross-validation. All three miRNAs showed very large effect sizes exceeding the minimum detectable effect at 80% power. Conclusions: In this pilot study, salivary miRNAs represent a hypothesis-generating candidate biomarker signal for BPD that requires external validation in larger, independent cohorts before any diagnostic or prognostic application can be considered. Full article

MicroRNAs are important regulators of melanoma progression; however, their relationship with cellular senescence remains poorly understood. To address this gap, a systematic review was conducted following PRISMA 2020 guidelines and prospectively registered in the International Prospective Register of Systematic Reviews (PROSPERO) under registration number CRD420251155760. A comprehensive search of PubMed, Scopus, Embase, and Dimensions identified studies evaluating melanoma-associated microRNAs and their effects on cell cycle regulation. Risk of bias was assessed using the SYRCLE tool and an adapted version of ToxRTool, with the included studies classified as having low, moderate, or high risk of bias. Fifteen studies met the eligibility criteria. Most studies reported that microRNA modulation reduced melanoma proliferation through cell cycle arrest; however, only two directly assessed senescence-associated markers. Of the fifteen identified microRNAs, seven had predicted targets and were included in the bioinformatic analysis. Integration of these predictions with genes downregulated in high-risk melanoma and underexpressed during cellular senescence identified 158 shared genes. Subsequent analysis identified predicted targets within this gene set only for hsa-miR-195-5p, and hsa-miR-425-5p, highlighting RNF138, and SYNCRIP as candidate regulatory genes. Collectively, these findings suggest a potential link between microRNA-mediated regulation and senescence-associated pathways during melanoma progression. Full article

Quince (Cydonia oblonga Mill.) is an important fruit crop, yet a systematic quality evaluation framework is lacking. This study comprehensively characterized multiple germplasms from distinct production areas. An integrated strategy combining physicochemical analysis, FT-MIR (Fourier transform mid-infrared spectroscopy), electronic nose (E-nose), headspace solid-phase microextraction–gas chromatography–mass spectrometry (HS-SPME-GC-MS), and chemometrics was employed. Significant variations were observed among accessions: certain varieties were observed to exhibit the highest pectin (1.86%) and total phenolic content (143.40 mg/100 g), while others showed superior firmness and titratable acidity. β-Damascenone in one accession was found to have an exceptionally high odor activity value (OAV) of 265.05. Multivariate analysis, including PLS-DA and OPLS-DA, effectively discriminated among quince accessions, with PLS-DA achieving 100% classification accuracy, and tentatively identified 18 key markers (VIP > 1) for accession discrimination. Loading scatter plot analysis further validated the contribution of these markers to the separation between accessions. However, due to the limited sample size (n = 18) and partial confounding between cultivar and origin, these findings should be considered exploratory and require validation in larger independent studies. This work provides preliminary insights into the diversity and geographical patterns of quality and flavor traits in quince germplasm, offering a preliminary foundation for germplasm evaluation and targeted utilization. Full article

Background/Objectives: Type 2 diabetes mellitus (DM) and carotid atherosclerosis are established risk factors for cardiovascular disease (CVD). However, their relative and combined prognostic significance in individuals without known CVD remains uncertain. This study aimed to evaluate the independent and combined associations of carotid plaques and DM with cardiovascular events and mortality in a high-cardiometabolic-risk primary prevention cohort. Methods: This prospective cohort study followed 6138 participants (3571 men [57%] and 2567 women [43%]; median age 53 years, IQR 48–58) enrolled in the Lithuanian High Cardiovascular Risk (LitHiR) primary prevention program from 2006 to 2023. All individuals underwent clinical assessment and carotid ultrasonography. Participants were stratified by DM status and the presence of carotid plaques. Associations with cardiovascular events, major adverse cardiovascular events (MACE, including non-fatal ischaemic stroke, non-fatal myocardial infarction, and cardiovascular death), and all-cause mortality were evaluated using Cox proportional hazards models. Results: During follow-up (median 6.5 years, IQR 4.5–9.0), 954 participants (16%) experienced composite cardiovascular events (MACE, including non-fatal ischaemic stroke, non-fatal myocardial infarction, and cardiovascular death). Bilateral carotid plaques were more common in individuals with cardiovascular events (23.3% vs. 19.4%; p = 0.007). Individuals with both DM and carotid plaques had the highest risk of MACE (HR = 1.696; 95% CI: 1.346–2.136; p < 0.001), myocardial infarction (MI; HR = 4.089; 95% CI: 1.590–10.516; p = 0.003), and all-cause mortality (HR = 1.802; p = 0.015). The presence of carotid plaques without DM was independently associated with increased risk of MACE (HR = 1.234; 95% CI: 1.062–1.433; p = 0.006) and MI (HR = 2.492; 95% CI: 1.176–5.278; p = 0.017), but not all-cause mortality (HR = 0.986; 95% CI: 0.689–1.413; p = 0.941). In contrast, DM without carotid plaques was not significantly associated with any outcome examined. Conclusions: In this high-cardiometabolic-risk primary prevention cohort, carotid plaques were independently and more strongly associated with cardiovascular outcomes than diabetes alone. Individuals with both carotid plaques and diabetes showed the highest observed risk of adverse cardiovascular events and all-cause mortality. These findings are associational and apply to a high-risk metabolic syndrome cohort; extrapolation to the general population requires further study. The results support the prognostic value of carotid plaque assessment as an adjunctive tool in cardiovascular risk evaluation. Full article

Background: Thoracic aortic aneurysm (TAA) is a potentially life-threatening degenerative disease whose principal danger arises from progressive aortic dilation with the attendant risk of rupture and dissection and which is characterized by extracellular matrix breakdown, smooth muscle loss, and endothelial dysfunction. Caveolae, plasma membrane microdomains built from caveolins (CAV1-3) and cavins (CAVIN1-4), govern nitric oxide (NO) signaling, endocytosis, and mechanotransduction. We hypothesized that downregulation of caveolae-associated genes, driven in part by microRNAs, contributes to endothelial failure and vascular remodeling in TAA. Methods: Normalized transcriptomic expression values for five caveolae-associated genes were retrieved from the GSE26155 dataset (43 TAA and 43 control aortas) using GEO2R. Differential expression was assessed for CAV1, CAV2, CAV3, CAVIN1, and CAVIN2, and Spearman correlation with Deming regression explored inter-gene relationships. Functional enrichment (Enrichr) and experimentally validated microRNA-target interactions (miRTarBase) were used to infer regulatory and mechanistic networks. CpG island mapping and gene-gene interactome construction (GeneMANIA) complemented the analyses. Results: CAV1 and CAV2 were downregulated in TAA at nominal significance (CAV1, p = 0.0225; CAV2, p = 0.0361); after Benjamini–Hochberg correction across the five candidate genes both differences attenuated to a consistent trend (q approximately 0.09), while the two caveolins were strongly co-expressed (Spearman r = 0.527, p < 0.001; Deming CAV2 = 1.881 × CAV1-0.892), indicating coordinated transcriptional regulation. Network analysis linked both genes to NOS3, NOSTRIN, EGFR, HRAS, and RAC1, consistent with impaired endothelial nitric oxide and GTPase signaling. Gene Ontology enrichment highlighted endothelial proliferation, nitric oxide metabolism, calcium homeostasis, vesicle organization, and MAPK regulation. Database-supported analysis (miRTarBase) identified miR-93-5p, miR-199a-3p, miR-203a-3p, and the miR-29 family as experimentally validated candidate repressors of CAV1/CAV2. Conclusions: This integrative transcriptomic and microRNA analysis identifies coordinated CAV1 and CAV2 downregulation as a candidate molecular event in thoracic aortic aneurysm, associated with caveolar loss, endothelial dysfunction, and disrupted nitric oxide homeostasis. The CAV1/CAV2-microRNA axis represents a candidate mechanistic signature warranting further investigation as a potential therapeutic target in aortic disease. Full article

This study investigated whether miR-31-5p abundance in fresh Holstein bull semen is associated with post-thaw sperm resilience. The initial cohort comprised 36 Holstein bulls, from which 16 ejaculates representing the highest- and lowest-ranking post-thaw freezers were selected for epigenetic and molecular analyses. Fresh semen was analyzed for miR-31-5p, while BAX and BCL2 were evaluated at transcript and protein levels before and after cryopreservation. Post-thaw sperm quality was assessed using total motility, viability, JC-1 mitochondrial membrane potential, Annexin-negative spermatozoa, reactive oxygen species (ROS) and sperm DNA fragmentation. Cryopreservation significantly impaired sperm quality, increased ROS and DNA fragmentation, and shifted the molecular profile toward increased BAX and reduced BCL2. Ejaculates with superior post-thaw motility showed higher miR-31-5p levels, accompanied by better preservation of viability, mitochondrial function, non-apoptotic membrane status, lower ROS burden and DNA fragmentation after thawing. Fresh miR-31-5p was positively associated with post-thaw motility, viability, mitochondrial function, and Annexin-negative spermatozoa and negatively associated with post-thaw ROS. Our data support miR-31-5p as a potential candidate biomarker of sperm freezability in Holstein bulls. Full article

Approximately half of Japanese patients with lung adenocarcinoma (LUAD) have epi-dermal growth factor receptor (EGFR) gene mutations. Therefore, EGFR is the most critical therapeutic target in treating LUAD. This study’s purpose is to explore novel therapeutic targets for LUAD and further improve EGFR inhibitor combination therapy. We created microRNA (miRNA) expression signatures from clinical specimens of LUAD patients harboring EGFR gene mutations using RNA sequencing. Based on the miRNA signature, we focused on miR-206, which had the most downregulated expression. We searched for its target gene in LUAD cells by facilitating transfection of miR-206 into the EGFR mutant cell line PC9 and searching for genes with suppressed expression. A total of 821 genes were downregulated in PC9 cells. Through molecular classification of these genes, we revealed that 18 genes were closely related to the cell cycle. Among these genes, we focused on cyclin-dependent kinase 4 (CDK4) and investigated the synergistic effects of a CDK4/6 inhibitor (abemaciclib or palbociclib) and osimertinib, an EGFR inhibitor in LUAD cells. In vitro and three-dimensional culture analyses showed that combination therapy with a CDK4/6 inhibitor and an EGFR inhibitor synergistically suppressed proliferation of LUAD cells with EGFR mutations. Our miRNA-based analysis is an excellent strategy for identifying therapeutic targets for LUAD. Continued analysis will reveal target molecules that enhance the therapeutic effects of EGFR inhibitors. Full article

Diabetic kidney disease (DKD) remains one of the most severe microvascular complications of type 2 diabetes mellitus (T2DM) and a leading cause of chronic kidney disease (CKD) worldwide. Nevertheless, despite considerable progress in elucidating its molecular background, early diagnosis and accurate stratification of disease progression remain challenging when relying on conventional clinical biomarkers such as albuminuria and estimated glomerular filtration rate (eGFR). Growing evidence indicates that DKD is driven by interconnected pathogenic mechanisms, including chronic hyperglycemia, activation of the protein kinase C (PKC) signaling pathway, renin–angiotensin–aldosterone system (RAAS) dysregulation, oxidative stress, inflammatory cascades, and immune system activation involving Toll-like receptors (TLR) and the NLRP3 inflammasome. These processes collectively contribute to endothelial dysfunction, podocyte injury, extracellular matrix accumulation, and progressive renal fibrosis. Exosomes and their molecular cargo, particularly miRNAs, have emerged as promising regulators and non-invasive biomarkers reflecting ongoing renal injury. Urinary exosomal microRNAs (uEV-miRNAs) are of interest due to their stability in biological fluids and their direct origin from nephron segments, enabling real-time reflection of renal pathophysiology. Accumulating studies suggest that differentially expressed microRNAs (miRNAs), including miR-21-5p, miR-30a-5p, miR-192-5p, and miR-142-3p, are closely associated with key pathways in DN. However, their clinical translation remains limited by methodological heterogeneity, the lack of standardized isolation protocols, and insufficient validation in large longitudinal cohorts. This review navigates the current landscape of knowledge on the molecular mechanisms underlying DKD and examines the emerging role of uEV-miRNAs as diagnostic biomarkers. Altogether, uEV-miRNAs offer a promising avenue for improving early detection, risk stratification, and disease monitoring in DKD. Full article

Background: Ligamentum flavum hypertrophy (LFH) is a major structural contributor to lumbar spinal stenosis and is characterized by extracellular matrix (ECM) remodeling with an increasingly recognized immune-associated component. However, the regulatory architecture linking disease-associated microRNA (miRNA) dysregulation to LFH transcriptomic remodeling remains incompletely defined. Methods: Public Gene Expression Omnibus datasets were analyzed using an integrated mRNA–miRNA transcriptomic framework. Single-cell RNA sequencing (GSE294458) was used to characterize the cellular landscape of hypertrophic and non-hypertrophic ligamentum flavum, whereas bulk transcriptomic analysis (GSE113212) identified LFH-associated differentially expressed genes. Differentially expressed miRNAs from an ossified ligamentum flavum dataset (GSE106256) were integrated with LFH-associated mRNA profiles through inverse miRNA–mRNA regulatory filtering. Functional enrichment, STRING protein–protein interaction (PPI) analysis, cytoHubba hub gene prioritization, LASSO regression, ROC analysis, remodeling-signature scoring, DGIdb, ChEA, and database-supported miRNA–target annotation were subsequently performed. Results: Single-cell analysis supported fibroblast-, myofibroblast-, and ECM-associated remodeling in hypertrophic ligamentum flavum. Bulk analysis identified nine significant differentially expressed genes, and integration with 33 dysregulated miRNAs generated 651 inverse-regulated core genes. Enrichment analyses highlighted ECM organization, proteoglycan/glycosaminoglycan (GAG) biology, immune cell differentiation, antigen presentation, and NF-κB/Wnt-related pathways. The STRING network included 650 nodes and 547 edges, with significant PPI enrichment (p = 2.04 × 10⁻¹⁴). LASSO prioritized PABPC1 and RPL4 as exploratory candidate hub features showing apparent discovery-cohort discrimination (AUC = 1.00); supplementary uncertainty, internal-stability, and separation-aware sensitivity analyses supported interpretation of this finding as a discovery-cohort signal rather than as independent diagnostic validation. Remodeling-signature analyses showed increased ECM fibrosis and proteoglycan/GAG scores, with inverse associations involving PABPC1 and RPL4. Multi-layer prioritization identified hsa-miR-708-5p as the leading candidate, followed by hsa-miR-23b-3p, hsa-miR-191-5p, hsa-miR-181a-5p, and hsa-miR-653-5p. Conclusions: This integrated mRNA–miRNA transcriptomic analysis delineated a coordinated fibrotic–immune remodeling landscape in LFH and prioritized experimentally testable miRNA candidates linked to network-central regulatory pathways. Full article

Nutrient supplementation may enhance muscle growth by supporting myogenic activity and regulating metabolic pathways involved in skeletal muscle development. However, the effect of specific nutrient supplementation on satellite cell (SC) activity and muscle-related metabolic pathways remains unclear. Two experiments were conducted to investigate dietary supplements, including guanidinoacetic acid (GAA), 5-hydroxytryptophan (5-HTP), and quercetin, on SC proliferation and differentiation in vitro and on muscle growth and transcriptomics in vivo. For the in vitro study, ovine SC were cultured with different levels (0, 12.5, 25, and 50 μmol/L) of 5-HTP, GAA, or quercetin to examine SC proliferation and differentiation. SC proliferation was greater with 5-HTP and quercetin supplementation, whereas GAA increased SC differentiation. Based on these results, 5-HTP and GAA were selected for the in vivo study because they increased proliferation and differentiation, respectively, and had a wider range of dose effectiveness (12.5 and 25 μmol/L). For the in vivo study, Texel lambs (n = 15; 33 ± 6 kg) were blocked by weight and assigned to one of three treatments: control, GAA, or 5-HTP for 28 d. Supplements were administered sublingually at a dose of 2.5 mg/kg body weight daily before feeding. GAA or 5-HTP did not influence (p > 0.05) average daily gain or dry matter intake. Longissimus muscle area was greater (p < 0.05) at the end of the study compared to the start for all treatment groups. mRNA sequencing showed that GAA supplementation altered gene expression (Padj < 0.05) compared to the control or 5-HTP. However, 5-HTP did not affect (p > 0.05) gene expression compared to the control. LC-MS also showed that plasma 5-hydroxyindoleacetic acid (5-HIAA) was elevated (p < 0.05) in the 5-HTP group. The results suggest that these dietary supplements can stimulate SC proliferation or differentiation in vitro. Short-term supplementation of GAA or 5-HTP in vivo did not alter growth performance, muscle mass, or miR-133a expression; however, GAA supplementation altered the transcriptome to promote amino acid metabolism pathways that are commonly linked to muscle growth through muscle protein synthesis and energy metabolism. Full article

Background/Objectives: Long non-coding RNAs (lncRNAs) are important regulators of tumor biology through their interactions with DNA, proteins, and non-coding RNAs. Although ENST00000615487.1 (also known as CTD-2396E7.11/AC010503.4) has been associated with multiple malignancies, its biological role in colorectal cancer (CRC) remains poorly characterized. This study aimed to investigate the expression pattern, cellular and subcellular localization, and potential functional role of ENST00000615487.1 in CRC using integrated in vitro and in silico approaches. Methods: Molecular characteristics of the transcript were obtained with the CPC2 and RNA Analyzer 3 tools. Differential expression of ENST00000615487.1 across 10 tumor types was analyzed using the UCSC Xena Browser. Transcript expression was experimentally evaluated in normal, tumor, and fibroblastic colon cell lines by PCR, while subcellular localization was assessed through the lncATLAS, lncLocator, and iLoc-LncRNA tools, and experimentally confirmed by qRT-PCR. Single-cell RNA sequencing data from the GSE161277 dataset were analyzed to determine cell type-specific expression patterns. Potential interactions with DNA, miRNAs, and proteins were investigated using Fasim-LongTarget, miRDB, and AnnoLnc2, followed by functional enrichment analyses using STRING and Enrichr. Results: ENST00000615487.1 was identified as a structurally stable non-coding transcript with a highly organized secondary structure. Differential expression analysis demonstrated significant downregulation in CRC compared with that in normal colon tissue. Single-cell transcriptomic analysis revealed predominantly epithelial-specific expression. In silico and experimental analyses demonstrated predominant nuclear localization in normal colon cells, whereas cytoplasmic enrichment was observed in CRC cells. Functional analyses identified potential interactions with HIP1R, RPH3AL, specific miRNAs, and proteins involved in transcriptional regulation and RNA processing pathways, as well as functional connections with proteins involved in vesicular transport. Conclusions: ENST00000615487.1 is a structurally stable lncRNA exhibiting context-dependent expression and localization patterns in CRC, suggesting a potential shift from nuclear transcriptional regulation toward cytoplasmic post-transcriptional functions during colorectal carcinogenesis. Full article