Altan, ZekiyeSahın, YunusKarabulut, AydınArslan, Ahmet2024-10-292024-10-2920232146-409Xhttps://doi.org/10.31832/smj.1187165https://search.trdizin.gov.tr/tr/yayin/detay/1186918https://hdl.handle.net/20.500.11776/13079Abstract Objective: MicroRNAs (miRNAs) are key regulators in the progression and development of hepatocellular carcinoma (HCC). In recent study the miR-4746 was found to be overexpressed in HCC, however, differential expression pattern and clinicopathological significance of miR-4746 in HCC remains unclear. In current study we aimed to evaluate expression profile, clinicopathological role and prognostic value of miR-4746 by using computational approaches. Material and Methods: The expression profile of miR-4746 in various human cancers was determined using the dbDEMC database. Also, we used ENCORI/Starbase v2 and UALCAN databases to analyze miR-4746 expression level in HCC. Moreover, we investigated clinicopathological function of miR-4746 by using UALCAN database. Finally, survival analysis was performed to determine prognostic significance of miR-4746 in HCC by Kaplan-Meier plotter and ENCORI/Starbase v2 databases. Results: The miR-4746 had differential expression patterns in various human cancers and was significantly upregulated in HCC tissues compared with normal samples. Clinicopathological analysis revealed that, miR-4746 was differentially expressed in different clinical parameters including cancer stage, tumor grade, nodal metastasis status, TP53 mutation status, and patient’s age. In addition, high expression of miR-4746 was significantly correlated with poor prognosis in HCC. Conclusion: Our findings indicated that miR-4746 might be as an oncogenic miRNA which were correlated with poor prognosis and worse clinicopathological outcomes. Furthermore, miR-4746 might have an important role in tumorigenesis of HCC and it might serve as potential prognostic biomarker.en10.31832/smj.1187165info:eu-repo/semantics/openAccessMiRNAprognosisbioinformaticshepatocellular carcinomamiR-4746Article1322162221186918