OBJECTIVE: Although multiple sclerosis (MS) is known to be an immune-mediated disease, very little is known about its etiopathogenesis. MicroRNAs (miRNAs) are small non-coding proteins involved in the regulation of gene expression. T-cell activation potential in neurodegenerative diseases has been a research topic of interest in recent years Cytokines play an important role in the course and pathogenesis of MS, The aim of the present study was to analyze expression levels of miR-20, miR-21, miR-26, miR-155, and Let-7, which target the cytokines interleukin IL-17 and IL-23, in order to evaluate the relationship between MS and miRNAs that modulate the expression of cytokines involved in the autoimmune pathway. MATERIALS and METHODS: The study included 20 relapsing-remitting multiple sclerosis (MS) patients who were at least 18 years of age and were undergoing outpatient immunomodulatory therapy and 20 healthy, unrelated individuals who had no systemic disease and were not taking any medication as a control group. Peripheral blood samples were collected from all participants into EDTA-containing tubes and plasma was isolated for cDNA synthesis. From these cDNA samples, miRNA expression levels were quantitatively analyzed via melting curve analysis using the miScript SYBR Green kit in real-time PCR device. RESULTS: Comparison of miRNA expression levels in the peripheral blood samples and MS patients and healthy subjects revealed that the MS patients had significant upregulation of miR-20 and downregulation of miR-26 and miR-155 compared to the control group (p<0.005). CONCLUSION: Dysregulation of miRNA expression may play a role in the pathogenesis of MS.

Background/Objectives: This study aimed to evaluate the relationship between sirtuin family members (SIRT1, SIRT3, and SIRT6) and Wnt/β-catenin pathways with inflammation during the rejection process following kidney transplantation, as well as to explore their potential roles as candidate biomarkers. Materials and Methods: Blood samples were collected from 35 kidney transplant rejection patients and 30 healthy controls. The gene expression levels of SIRT1, SIRT3, SIRT6, and Wnt/β-catenin pathway components were measured using real-time PCR, and miRNA and lncRNA expression levels were analyzed. Statistical analyses were performed using SPSS version 23. Results: Significant alterations in SIRT1, SIRT3, and SIRT6 expression levels were observed in rejection patients, suggesting their potential role in disease pathogenesis and as therapeutic biomarkers. Key altered genes included hsa-miR-34c-1, hsa-miR-122b-5b, MALAT1, HOTAIR, LINC00473, TUG, PVT1, SIRT1, SIRT3, SIRT6, WNT1, TCF-LEF, LRP, AXIN1, IL1B, IL6, and IFNB1, all showing significant changes. However, no significant differences were found for miRNAs such as hsa-miR-21-2, hsa-miR-155-5p, and hsa-miR-200b-3p. SIRT1 expression was significantly decreased in the cellular rejection group, with a more pronounced reduction in these patients. Significant differences in SIRT1 expression were observed with interstitial inflammation and glomerulitis. Increased inflammation severity correlated with decreased SIRT1 and increased TCF-LEF, TUG, and miR-21 levels, while tubulitis severity was associated with elevated TCF-LEF and miR-155 expression. Conclusions: Along with the activation of Wnt/β-catenin pathways and increased levels of certain miRNAs and long non-coding RNAs (lncRNAs) associated with TCF-LEF transcription factors, the observed decrease in SIRT1 expression may be related to the severity of inflammation and tubulitis. These findings suggest that SIRT1, Wnt/β-catenin pathways, and non-coding RNAs play a role in the rejection process following kidney transplantation and could be considered as potential biomarkers or therapeutic target candidates for future research.

Objective: This prospective case-control study aimed to assess the predictive value of the expression levels of Hsa-miR-200-3p, Hsa-miR-155-5p, Hsa-miR-20a-5p, Hsa-miR-221-3p, Hsa-miR-34a-5p, Hsa-let-7b-5p, and Hsa-miR-125b-5p microRNAs (miRNAs) in the diagnosis, prognosis, and treatment response of hepatocellular carcinoma (HCC) patients. The study includes 20 healthy controls and 25 HCC patients. Methods: The study was designed as a prospective case-control study and was conducted between 2023 to 2024 at Ataturk University, in collaboration with the Departments of Organ Transplantation, Medical Biology and Medical Pathology. miRNA expression levels were examined in HCC tissue samples. RNA was extracted from paraffin-embedded tissues, and miRNA expression levels were measured using reverse transcription-quantitative PCR. The relationships between clinical factors and miRNA expression levels were assessed. Results: Significant differences in expression levels were found between HCC tissues and healthy control tissues for Hsa-miR-20a-5p, Hsa-miR-125b-5p, and Hsa-let-7b-5p. A significant correlation was observed between Hsa-miR-34a-5p and γ-glutamyl transferase levels (P<0.05), as well as between Hsa-miR-20a-5p and albumin levels (P<0.05). Significant differences in expression levels were found between patients with and without HBV infection for let-7b-5p (P=0.007) and miR-200-3p (P=0.013). Conclusion: This study demonstrates that miRNAs, particularly Hsa-miR-20a-5p and Hsa-miR-34a-5p, may regulate the Wnt/β-catenin pathway and influence the progression of HCC. Disease progression was assessed by comparing miRNA expression levels with clinical markers (such as γ-glutamyl transferase and albumin). High expression of Hsa-miR-20a-5p affects the Wnt/β-catenin pathway and plays a significant role in disease processes. Additionally, the correlation between Hsa-miR-34a-5p and γ-glutamyl transferase indicates disease progression. However, further advanced studies are required to better understand how the Wnt/β-catenin pathway is regulated by miRNAs and the impact of this regulation on the disease. doi: https://doi.org/10.12669/pjms.41.5.11444 How to cite this: Altundas N, Balkan E, Kizilkaya M, Demirci E. Exploring the role of miRNAs in Hepatocellular Carcinoma: Insights into signaling pathways and their regulatory mechanisms. Pak J Med Sci. 2025;41(5):1441-1446. doi: https://doi.org/10.12669/pjms.41.5.11444 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This prospective cross-sectional study aimed to evaluate leukocyte DNA damage in coronavirus disease (COVID-19) patients. In this study, 50 COVID-19-positive patients attending the Erzurum City Hospital Internal Medicine Outpatient Clinic and 42 control group patients were included. DNA damage was detected in living cells through leukocyte isolation in 50 COVID-19-positive patients using the comet assay method. DNA tail/head (olive) moments were evaluated and compared. White blood cells (WBC), red blood cells (RBC), hemoglobin (HGB), neutrophils (NEU), lymphocytes (LYM), eosinophils (EO), monocytes (MONO), basophils (BASO), platelets (PLT), and the neutrophil/lymphocyte ratio (NLR) were analyzed. The RBC, lymphocyte, eosinophil, and monocyte means were significantly higher in the control group (p < 0.05), whereas the HGB and neutrophile means were significantly higher in the study group (p < 0.05). There were significant negative correlations between COVID-19 and RBC (r = −0.863), LYM (r = −0.542), EO (r = −0.686), and MONO (r = −0.385). Meanwhile, there were significant positive correlations between COVID-19 and HGB (r = 0.863), NEU (r = 0.307), tail moment (r = 0.598), and olive moment (r = 0.582). Both the tail and olive moment mean differences were significantly higher in the study group, with higher ranges (p < 0.05). COVID-19 infection caused statistically significant increases in both the tail and olive damage percentage in patients, causing DNA damage. Lastly, the NLR rate was associated with the presence and progression of COVID-19.

Objective: This study investigates the role of Epstein-Barr virus (EBV)-derived microRNAs (miRNAs) in the pathogenesis of multiple sclerosis (MS), aiming to elucidate their impact on immune-related molecular mechanisms. Methodology: This study was conducted at Ataturk University (Departments of Neurology and Medical Biology), between July 2022 and March 2025, the study included 40 MS patients and 40 healthy controls. Peripheral blood RNA samples were analyzed using Real-Time PCR to measure EBV miRNA and host mRNA expression. Data were evaluated using SPSS v23. Results: EBV-derived miRNA levels were significantly elevated in MS patients. Specifically, BART17-5p, BART10-5p, BHRF1-3 and BART5-3p levels were markedly increased (p<0.001). BART8-5p showed a negative correlation with CREB1 (r=-0.419; p=0.021), suggesting suppression of host signaling pathways. Immune markers such as CXCL3, MALT1, IFNB1, IL6, IL2 and FOXP3 also differed significantly between groups (p=0.005). Moderate correlations were noted between EBV-miRNAs and immune genes (e.g., IFNB1 and BART10-5p: r=0.433; p=0.017). Weak negative correlations were found between BART8-5p and multiple immune-related genes (e.g., IL1B, STAT3, CD4) and between BART19 and IL2 (r=-0.373; p=0.043). Logistic regression revealed that increased BART miRNA levels were associated with elevated MS risk. Conclusion: EBV-derived miRNAs are linked to immune activation and may contribute to MS pathogenesis. These miRNAs may serve as potential biomarkers and therapeutic targets in MS management.