Esophageal cancer (EC) ranks among the eight most common malignancies worldwide. Long noncoding RNAs LINC00472 and LINC02381 are implicated in cancers, but their role in EC remains unclear. Therefore, this study investigates the roles of LINC00472 and LINC02381 in EC. This study analyzed lncRNA, miRNA, and mRNA sequencing related to EC using TCGA. Then, the LINC00472, LINC02381, hsa-miR-7-5p, and FHIT genes were identified. Expression levels of these genes were assessed in 20 EC tissue pairs using RT- qPCR, while FHIT protein expression was examined by Western blot and Immunohistochemistry. Chi-square tests explored clinicopathological correlations, while ROC analysis evaluated their diagnostic potential. Bioinformatic analysis and RT-qPCR results demonstrated significantly decreased expression of LINC00472, LINC02381, and FHIT (p<0.01), alongside increased hsa-miR-7-5p expression in EC (p<0.0001). A significant reduction in FHIT protein expression was also observed (p<0.01). Correlations showed that LINC02381 and FHIT expressions were positively correlated, while LINC00472 and LINC02381 were negatively associated with hsa-miR-7-5p (p<0.05). Elevated levels of hsa-miR-7-5p were significantly linked to vascular invasion and deeper muscularis propria infiltration in EC (p<0.05). Higher FHIT levels were also linked to increased necrosis and decreased vascular invasion (p<0.05). The ROC analysis demonstrated measurable AUC values for each of the examined genes, suggesting potential diagnostic relevance that warrants further validation. This research revealed dysregulated genes LINC00472, LINC02381, hsa-miR-7-5p, and FHIT in EC, proposing a regulatory network through bioinformatic analyses and correlations. Results establish groundwork for functional studies, emphasizing their potential significance in understanding and controlling EC pathogenesis.
Colorectal cancer is often associated with endocrine and metabolic disturbances. These alterations reflect interactions between the tumor and the host. The aim of this study was to evaluate hormonal, metabolic, and trace-element profiles in male patients with colon cancer (stages I-III). The associations between these biomarkers and disease stage were also examined. In this cross-sectional, case-control study, 300 histopathologically confirmed male patients with colon cancer (stages I-III) and 100 age-matched healthy controls (50-70 years) were enrolled. Serum levels of thyroid hormones (T3, T4, TSH), parathyroid hormone (PTH), parathyroid hormone-related peptide (PTHrP), calcium, vitamin D, insulin-like growth factor-1 (IGF-1), (3-catenin, ferritin, and trace elements (Zn, Cu, Se, Mg, Mn) were measured using enzyme-linked immunosorbent assay and atomic absorption spectrophotometry. Statistical analyses including one-way ANOVA component analysis, and multivariate regression were used. Several endocrine and metabolic markers differed significantly between cancer patients and controls. Compared with controls, cancer patients showed thyroid dysfunction, reduced PTH with elevated calcium and PTHrP, pronounced vitamin D deficiency, and higher IGF-1 and magnesium, manganese, and ferritin levels alongside elevated copper concentrations. Multivariate analyses revealed stage-related biomarker patterns and complex relationship among markers. Colon cancer in men was associated with coordinated endocrine, metabolic, and trace-element alterations detectable from early stages, supporting the value of integrated biomarker profiling.
Metabolomics, the comprehensive analysis of small-molecule metabolites within biological systems, has emerged as a powerful analytical platform for advancing the diagnosis, prognosis, and management of infectious diseases. Leveraging highthroughput technologies such as mass spectrometry (MS) and nuclear magnetic resonance (NMR), metabolomics enables the identification of distinct metabolic fingerprints associated with infections, offering novel metabolomic insights hostpathogen interactions and disease pathophysiology. MS-based platforms, coupled with chromatographic techniques like gas chromatography (GC-MS) and liquid chromatography (LC-MS), provide exceptional sensitivity and specificity for metabolite detection in biofluids such as blood, urine, and cerebrospinal fluid (CSF). NMR spectroscopy complements these approaches by enabling non-destructive, reproducible analyses ideal for longitudinal studies and treatment monitoring. In infectious disease diagnostics, metabolomics has demonstrated the ability to differentiate bacterial, viral, and fungal infections through unique metabolic signatures. For example, bacterial sepsis is characterized by significant perturbations in lipid metabolism, including alterations in phospholipids and sphingolipids, which correlate with systemic inflammation and immune activation. Beyond diagnostics, metabolomics contributes to understanding antimicrobial resistance (AMR) by profiling metabolic reprogramming in resistant strains, revealing mechanisms such as increased efflux pump activity, biofilm formation, and membrane remodeling. These insights present potential therapeutic targets and inform personalized treatment strategies. The integration of metabolomics with genomics and proteomics further enhances diagnostic and prognostic accuracy. This review details infections (RTIs), UTIs, and Helicobacter pylori (H. pylori) infections, emphasizing its potential to revolutionize infection management while discussing current challenges and future directions.
Fat build-up can lead to inflammation, which in turn exacerbates health conditions and intensifies complications associated with obesity. This is also related to obesity related gene factors, the FTO gene, which is thought to increase visceral fat. This review investigates the relationship between FTO gene polymorphisms rs9939609 and rs1421085 and visceral fat accumulation. A systematic review was carried out through searches in PubMed, Science Direct, and Cochrane databases, from the index date from 2010 to October 2024. Studies with case control, cohort, and cross-sectional designs that discussed the relationship between FTO gene polymorphisms rs9939609 and rs1421085 and increased risk of visceral fat in obese patients were included in this study. This study included 19.732 samples from 11 cohort, case-control, and cross-sectional studies. Five studies revealed that the A allele of rs9939609 and the T allele of rs1421085 were significantly associated with increased visceral fat levels. Findings on the involvement of FTO gene polymorphisms rs9939609 and rs1421085 in visceral fat risk remain inconclusive and warrant further investigation. Therefore, we as researchers support further research that includes the role of this gene in visceral fat using analysis so that it can confirm more precise results in statistics.
Although mucin-producing carcinomas of the gastrointestinal tract and breast have similar histological characteristics, their clinical behavior and prognosis vary. The relationship of mucin gene product expression in the development of these clinical differences is poorly understood. This study examines the histopathological characteristics of gastrointestinal and breast mucin-producing carcinomas for the expression of MUC1, MUC2, MUC4, and MUC5AC and their relationship to patient outcome. A retrospective comparative study of 120 mucinous carcinomas of the gastrointestinal tract and breast (60 in each group) was conducted. The histopathological characteristics of the tumors were examined. MUC gene expression was quantified by RT-qPCR in a subset of 60 cases. Overall survival was evaluated in the RT-qPCR subset using Kaplan-Meier analysis and multivariate Cox proportional hazards models. Gastrointestinal tumors exhibited significantly higher histologic grade and greater necrosis compared with mammary tumors (P < 0.01). MUC2 and MUC5AC were markedly overexpressed in gastrointestinal carcinomas (P < 0.001 for both), whereas MUC1 and MUC4 were expressed across both tumor types. In multivariate analysis, high expression of MUC1 (hazard ratio = 2.18; 95% confidence interval [CI], 1.31-3.61; P = 0.003) and MUC4 (HR = 1.89; 95% CI, 1.10-3.23; P = 0.017) was independently associated with reduced overall survival. In contrast, MUC2 and MUC5AC expression distinguished tumor origin but showed no prognostic significance (P > 0.05). Mucin gene expression profiles differ substantially between GI and mammary mucin-rich carcinomas. MUC1 and MUC4 have prognostic relevance, while MUC2 and MUC5AC aid in determining tumor origin. Integrating histopathological evaluation with molecular profiling may improve diagnostic accuracy and risk stratification in mucin-rich carcinomas.
The DNA damage response (DDR) safeguards genomic integrity through lesion sensing, checkpoint activation, and repair. While ATM/ATR-centered DDR signaling is well defined, how growth-associated pathways such as MAPK/ERK and PI3K/AKT coengage with DDR programs across distinct genotoxic stresses remains incompletely resolved. U2OS and HCT116 cells were challenged with ionizing radiation (4 Gy), replication stress (hydroxyurea, 2 mM), or oxidative stress (H2 O2 , 200 & micro;M, 30 min). DDR and growth-pathway phosphorylation kinetics were quantified by immune-blot dynamics were assessed by DNA fiber assays under HU with ATR or PI3K inhibition. DNA damage burden was measured by alkaline comet tail moment and 53BP1 foci at 6 h and 24 h. Long-term proliferative capacity was quantified by clonogenic survival (SF4) after IR. Pharmacologic perturbations included trametinib (MEK), BKM120 (PI3K), VE-821 (ATR), NU7441 (DNA-PK), and olaparib (PARP). Analyses used biological replicate-level inference. Stressors produced expected checkpoint signatures (IR: ATM- CHK2; HU: ATR-CHK1) with temporally overlapping ERK and AKT phosphorylation changes. ATR inhibition markedly increased fork stalling and reduced fork progression under HU. PI3K inhibition was associated with higher early DNA-damage readouts (comet tail moment and 53BP1 foci at 6 h) and produced larger reductions in clonogenic survival after IR than MEK inhibition in both cell lines. Canonical DDR activation and growth-signaling phosphorylation changes co-occur after genotoxic, replication, and oxidative stress and are associated with distinct functional outcomes: ATR predominates in fork stability, whereas PI3K activity is linked to early damage burden and post-IR survival. These findings motivate mechanistic follow-up to define causal nodes for combination targeting in genomically unstable cells.
This study investigated the combined antibacterial and anti-biofilm effects of zinc oxide nanoparticles, iron oxide nanoparticles, and a newly isolated bacteriophage, BacPhageSAU27, against Staphylococcus aureus SAU27as a multidrug-resistant strain. The study aimed to evaluate the potential synergistic effects of phage-nanoparticle combinations in combating biofilm-related infections caused by multidrug-resistant S. aureus. S. aureus was cultured and evaluated for biofilm formation. BacPhage-SAU27 was isolated from wastewater using the double-layer agar method and characterized by plaque assays. The minimum inhibitory concentration of zinc oxide nanoparticles and iron oxide nanoparticles was determined individually and in combination, and BacPhage-SAU27 was added to assess interaction effects. Biofilm formation and destruction were analyzed using crystal violet staining and scanning electron microscopy, and the fractional inhibitory concentration index was calculated. The minimum inhibitory concentrations for zinc oxide nanoparticles and iron oxide nanoparticles were 120 & micro;g/mL and 72 & micro;g/mL, respectively. The combination of both nanoparticles reduced the minimum inhibitory concentration to 25 & micro;g/mL. Adding BacPhage-SAU27 further reduced the minimum inhibitory concentration to 15 & micro;g/mL for zinc oxide nanoparticles and 18 & micro;g/mL for iron oxide nanoparticles and lowered the multiplicity of infection to 0.00001. BacPhageSAU27 alone and in combination with nanoparticles significantly inhibited biofilm formation and caused biofilm destruction. Scanning electron microscopy confirmed damaged biofilm structures and complete bacterial clearance with the phage- nanoparticle combination. The combination of BacPhage-SAU27 with zinc oxide and iron oxide nanoparticles offers a promising strategy to combat S. aureus biofilms and may provide an alternative to antibiotic therapies.
Gold nanoparticles (AuNPs) are a suitable choice in the biomedical field due to their physical properties. The presence of gold nanoparticles, acting alongside mesenchymal stem cells (MSCs) through paracrine interactions, accelerates wound closure, enhances angiogenesis, favorably regulates extracellular matrix remodeling, and encourages skin regeneration with typical construction and function. In this study, we hypothesized that AuNPs Nano scaffolds would enhance the proliferation and specialization potential of human adipose-derived mesenchymal stem cells (hADSC in the wound area during in vitro, In vivo studies. To evaluate the nanoparticles; transmission electron microscopy was used to detect AuNPs and dynamic light scattering assay was used to estimate their size. Immunofluorescence staining, MTT assay, and semi-quantitative histological analysis were performed. Our results show that AuNPs at non-toxic concentrations (6 ppm) improve collagen content deposition and micro vessels expression induces cell migration and therapeutic efficacy in wound healing by hADSC at 14 and 28 days after surgery. As a result, AuNPs promote differentiation through a paracrine signaling pathway. Therefore, hADSC cultured with AuNPs can be used as a reagent to enhance skin tissue formation.
Dental implant integration is dependent on osteogenesis driven by the transcription factor SATB2, which regulates osteogenic genes. MicroRNAs (miRNAs) modulate SATB2 and influence bone formation. This review evaluates miRNA-SATB2 interactions, non-coding RNAs, and biomaterials in dental implant osseointegration. A critical review of studies from 2015 to 2025 was conducted to elucidate miRNA-SATB2 interactions and their impact on osteogenesis. Inhibitory miRNAs (e.g., miR-31, miR-140-5p) suppress SATB2 via the Wnt/β-catenin or SIRT1/Smad3 pathways and reduce osteoblast differentiation. Promoter miRNAs (e.g., miR-17-5p, miR-27a-5p) enhance SATB2 through BMP/Smad signaling. Non-coding RNAs (e.g., lncRNA H19, hsa_circ_0007292) inhibit miRNAs affecting cancellous bone and promote osteogenesis. Biomaterials such as collagen/nanohydroxyapatite (Col/nHA) scaffolds and comorbidities (e.g., osteoporosis) influence outcomes. Inconsistent miRNA roles and limited in vivo data are key gaps. miRNA- SATB2 interactions are critical for implant success. Patient-specific miRNA profiling and targeted therapies hold promise, pending clinical validation.
Orthodontic tooth movement (OTM) is a complex biological process involving the precise remodeling of alveolar bone in response to mechanical forces. This remodeling is mediated by the coordinated activities of osteoblasts (responsible for bone formation) and osteoclasts (responsible for bone resorption) within the periodontal ligament (PDL). Mechanical stimuli are transduced into biochemical signals, which regulate cellular behavior through key signaling pathways such as RANKL/RANK/OPG and Wnt/β-catenin. MicroRNAs (miRNAs), as crucial post-transcriptional regulators of gene expression, play significant roles in skeletal development and bone homeostasis. They influence essential signaling cascades that govern the differentiation, function, and survival of osteoblasts and osteoclasts. Among them, miR-214 and miR-206 have emerged as potent negative regulators of osteoblast differentiation. This review focuses on how their common target, EphrinA2, plays a pivotal role in bone remodeling. EphrinA2 is a membrane-bound ligand critical for osteoclast-osteoblast communication. Upon binding to its receptor EphA2 on osteoblasts, EphrinA2 promotes osteoblast differentiation and bone formation. Dysregulation of the miR-214/miR-206-EphrinA2 axis impairs osteoblast function, disrupts bone remodeling, and can adversely affect the rate and stability of OTM. In conclusion, elucidating the regulatory functions of miR-214 and miR-206 and their modulation of EphrinA2 provides valuable insights into bone remodeling dynamics during OTM. Targeted manipulation of this pathway holds promise for developing novel molecular therapies that aim to enhance the efficacy, speed, and long-term stability of orthodontic treatments, while also addressing broader skeletal pathologies associated with disrupted bone remodeling.
This study investigated the effects of chemically synthesized gold nanoparticles (GNPs) and green gold nanoparticles (gGNPs) derived from Achillea biebersteinii extract on antrum diameter and the expression of genes associated with follicular development in NMRI mice. Female mice were treated with GNPs and gGNPs at concentrations of 10, 50, and 100 µg/mL. Antrum diameter in ovarian follicles was measured using ImageJ software. Gene expression levels of BMP-15, GDF-9, SOD, and GPx were quantified via real-time PCR.Treatment with gGNPs at 100 µg/mL significantly increased the antrum diameter of secondary follicles compared to GNPs (p ≤ 0.05), while no significant changes were observed in grafted follicles. A dose-dependent upregulation of BMP-15, GDF-9, GPx, and SOD was observed in both GNP and gGNP groups, with gGNPs eliciting stronger effects across all genes (p ≤ 0.05). The findings suggest that A. biebersteinii-mediated green synthesis enhances the biological activity of GNPs, particularly in promoting follicular development and antioxidant gene expression. Although mechanistic pathways were not explored in this study, future research should address these gaps and evaluate long-term safety and therapeutic potential.
Pulmonary toxoplasmosis is a rare but potentially fatal opportunistic infection, most often reported in HIV-infected individuals. Its occurrence in non-HIV immunocompromised patients-particularly those with hematologic malignancies like multiple myeloma (MM)-is exceedingly rare and diagnostically challenging due to nonspecific clinical and radiologic features. While Toxoplasma gondii infection is typically mild in immunocompetent hosts, it can cause severe disease in immunocompromised populations. A literature review was conducted using PubMed, Scopus, and Google Scholar (January 2000-May 2025) with keywords: 'pulmonary toxoplasmosis,' 'multiple myeloma,' 'non-HIV,' 'immunocompromised,' and 'BAL PCR.' Only English-language case reports and reviews were included, with emphasis on studies from endemic regions and the past five years. We report a 49-year-old Iranian man with newly diagnosed IgG kappa MM who presented with fever, chills, vomiting, and dyspnea. Chest CT revealed a 4.2 × 3.8 cm consolidation in the posterior segment of the right lower lobe. T. gondii infection was confirmed via bronchoalveolar lavage (BAL) through tachyzoite detection on Giemsa stain and molecular identification using qPCR and nested PCR targeting the Gra6 gene. He showed transient clinical improvement and was discharged on hospital day 7. Unfortunately, he died at home within 48 hours due to MM progression, before anti-toxoplasmosis therapy was initiated. This case underscores the diagnostic difficulty of pulmonary toxoplasmosis in non-HIV immunocompromised patients and the importance of molecular BAL testing. Prophylactic measures such as co-trimoxazole should be considered in high-risk MM patients. Guidelines must address screening and management in this vulnerable population.
Although biofilms on endotracheal tube (ET) surfaces represent a major clinical challenge, studies addressing the effect of lytic bacteriophages on these biofilms are relatively scarce. This study focused on examining the anti-biofilm capability of three specific phage against an XDR isolate of Acinetobacter baumannii in a 48-hour preformed biofilm on an ET surface. For this purpose, crystal violet staining, colony counting, and scanning electron microscopy (SEM) were employed. The results demonstrated a significant decrease in biofilm mass and bacterial count after 24 hours of exposure to the phage cocktail. SEM images confirmed a dramatic reduction in the biofilm. Based on these findings, phage therapy has the potential to reduce and disrupt biofilms on ET surfaces.
Trace amine-associated receptor 1 (TAAR1) is a classical representative of G-protein coupled receptors (GPCRs). It is widely distributed in the mammalian brain, potentially plays an important role in modulating neurotransmitter functions and may regulate synaptic transmission and neuronal activity. Studies on TAAR1 signaling pathways were reviewed to identify the potential of TAAR1 as a novel target for neuroprotection and neurorepair. TAAR1 realizes effects through binding to the G-protein subunits Gas or Ga13. The target of Gas is PKA and the target of Ga13 is RhoA. Among the RhoA-mediated effects of TAAR1, effects on MAPK/ERK pathway kinases, AMPA and NMDA glutamate receptors and CREB factor have been investigated. RhoA-mediated effects include effects on the internalization of DAT and EAAT3, neuronal transporters of dopamine and glutamate. A G-protein independent pathway is mediated by β-arrestin and is probably related to the formation of the TAAR1-D2R heterodimer. The modulatory effect of TAAR1 on neurotransmitter systems allows us to consider TAAR1 agonists as potential therapeutic agents for the treatment of neurodegenerative diseases and psychiatric disorders, as well as neuroprotectors in ischemic brain damage.
Prior research has indicated a potential link between the miR-146a rs2910164 genetic variant and an individual's susceptibility to pulmonary tuberculosis (TB). Nevertheless, the evidence from various studies is contradictory and has not yielded a consensus. This meta-analysis was therefore conducted to systematically assess the relationship between this specific single nucleotide polymorphism (SNP) and the risk of developing tuberculosis. A systematic literature search was performed utilizing the electronic databases PubMed, Web of Science, Scopus, and ISI to capture all relevant publications available through April 2024. To ensure comprehensive coverage, the reference lists of retrieved full-text articles were also manually scrutinized. For the quantitative synthesis, pooled odds ratios (ORs) with their corresponding 95% confidence intervals (CIs) were computed to determine the overall effect estimates. The chi-square (χ²) test and the I² statistic were applied to assess and quantify heterogeneity. This meta-analysis included 6363 individuals (2904 TB patients and 3459 healthy controls) from eight case-control studies. The pooled effect estimates across all genetic inheritance models (e.g., dominant model: OR = 0.971, 95% CI: 0.884-1.068) did not reveal a significant link between the rs2910164 polymorphism and susceptibility to tuberculosis. The analysis revealed considerable heterogeneity across most genetic models, as indicated by I² statistics exceeding 70%. Conversely, statistical tests found no evidence of publication bias. The collective evidence from this analysis does not support a significant association between the miR-146a rs2910164 G>C variant and tuberculosis susceptibility. Confirmation of this null association necessitates future validation in large-scale, rigorously designed studies.
Chronic kidney disease (CKD) is frequently accompanied by disturbances in bone metabolism, leading to a heightened risk of fractures. The receptor for advanced glycation end-products (RAGE) plays a pivotal role in the pathogenesis of CKD. This case-control study included 50 CKD patients and 50 healthy controls to examine the association between RAGE gene polymorphisms (rs2070600 and rs2071288) and bone metabolism markers. Serum parathyroid hormone (PTH), alkaline phosphatase (ALP), and vitamin D levels were measured as indicators of bone metabolism. CKD patients exhibited significantly higher ALP (317.54 ± 21.95 U/L) and PTH (331.33 ± 17.11 pg/mL) levels, along with lower vitamin D (26.92 ± 6.64 ng/mL) compared to controls (all P < 0.05). The CC genotype of rs2070600 was more prevalent among patients (52%) and was associated with an increased risk of CKD (OR = 2.79, 95% CI: 1.21-6.39, P = 0.014). In contrast, no significant association was found between rs2071288 and CKD risk. Notably, individuals carrying CC or CT genotypes for rs2070600 and rs2071288 had higher levels of PTH and ALP, alongside significantly lower levels of vitamin D. The RAGE gene's rs2070600 polymorphism may be connected to abnormalities in bone metabolism and the advancement of CKD. These results indicate that rs2070600 genotyping may be useful in identifying high-risk patients; however, additional research is required to validate its clinical significance.
Atherosclerosis is the primary cause of death in developed nations. The key risk factors for atherosclerosis are inflammation and lipid disorders which may all be influenced by microRNAs (miRs). This study evaluated the correlation between miR-20a-5p, miR-124-3p, miR-125b-5p, and key atherogenic and inflammatory genes (TLR4, Resistin, CD36, TNF-α) in PBMCs from patients with angiography-proven atherosclerosis. 45 healthy individuals and 45 atherosclerosis patients were selected. After sampling patients and isolating in peripheral blood mononuclear cell (PBMC) cells, gene levels were measured using real-time polymerase chain reaction. In the atherosclerosis patient group, Toll-like receptor 4 (TLR4) and Resistin were upregulated compared to the control group (p <0.05). Conversely, miR-20a was downregulated in patients and inversely correlated with fasting blood glucose (p <0.05). Additionally, miR-124 expression with Resistin had a significant negative correlation (p <0.05). The study confirmed that the expression level of miR-125b levels may serve as a potential biomarker for atherosclerosis (p <0.01). The reduction of miR-20a was related to the risk of developing atherosclerosis (p <0.05). miR-20a, miR-124, and miR-125b present promising therapeutic targets for atherosclerosis. Since atherosclerosis has no specific clinical symptoms and early diagnosis is very important, the diagnostic biomarker miR-125b has the potential to significantly aid in the early detection of various diseases with an area under the curve (AUC) of 0.74, 52% sensitivity, and 74% specificity. In addition, the measurement of miR-20a helps determine the progression of atherosclerosis risk.
Breast cancer (BC) remains the leading cause of cancer-related mortality in women worldwide, primarily due to its high invasiveness and therapeutic resistance. This study explores the role of noncoding RNAs, circular RNAs (circRNAs), in BC progression through a competing endogenous RNA (ceRNA) network. Three GEO circRNA microarray datasets (GSE101123, GSE165884, GSE182471) were retrieved, normalized, and batch-corrected using ComBat. Differentially expressed circRNAs (DEcircRNAs) were identified via limma (|log₂FC| > 1, FDR < 0.05). Differentially expressed miRNAs (DEmiRNAs) and mRNAs (DEgenes) were derived from TCGA-BRCA RNA-Seq (1,091 tumors, 113 normals) and miRNA-Seq (1,078 tumors, 104 normals) data using DESeq2 (|log₂FC| > 1, FDR < 0.05). CircRNAs harboring miRNA response elements (MREs) were selected via CSCD, and miRNA-mRNA interactions predicted through TarBase, prioritizing upregulated DEgenes. A ceRNA network was constructed in Cytoscape based on expression concordance. The hsa_circ_0000378/hsa-miR-205-5p/RAD51 axis was validated in 48 paired BC and adjacent non-tumor tissues by RT-qPCR. Results indicated hsa_circ_0000378 upregulation (2.74-fold, p<0.001), hsa-miR-205-5p downregulation (0.64-fold, p=0.0022), and RAD51 upregulation (3.46-fold, p<0.001) in tumors. Spearman correlations showed negative associations between hsa_circ_0000378 and hsa-miR-205-5p (r = -0.474, p<0.001), hsa-miR-205-5p and RAD51 (r = -0.383, p<0.001), and positive between hsa_circ_0000378 and RAD51 (r = 0.497, p<0.001), supporting ceRNA regulation. ROC analysis revealed RAD51's diagnostic potential (AUC=0.83, 95% CI: 0.74-0.90, sensitivity=0.81, specificity=0.55), followed by hsa_circ_0000378 (AUC=0.75, 95% CI: 0.65-0.85, sensitivity=0.71, specificity=0.77), and hsa-miR-205-5p (AUC=0.66, 95% CI: 0.56-0.76, sensitivity=0.69, specificity=0.55). These results propose the hsa_circ_0000378/hsa_miR-205-5p/RAD51 axis as a potential biomarker; mechanistic validation and larger cohorts are needed for clinical application.
