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Differential Expression and Pathological Implications of Linc01089 and Linc01578 in Acute Myeloid Leukemia Publisher



Khosroabadi Z1 ; Sharifi M1 ; Salehi M1 ; Mehrzad V2
Authors
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Authors Affiliations
  1. 1. Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Internal Medicine, Division of Hematology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Gene Reports Published:2025


Abstract

Background: Acute myeloid leukemia (AML) is a type of blood cancer that has an outlook emphasizing the importance of finding treatment targets. This research delves into the differences in expression of different types of coding RNAs in AML, specifically focusing on Linc01089 and Linc01578. Methods: We carried out an analysis using AML datasets to pinpoint non-coding RNAs showing significant expression differences. Subsequently, we used PCR (qPCR) on samples from AML patients and healthy individuals to validate our discoveries. Furthermore, we used weighted gene co-navigation analysis (WGCNA) to investigate the pathways and key genes associated with these non-coding RNAs. Results: Our analysis revealed a decrease in the levels of Linc01089 and Linc01578 in AML samples compared to those from individuals. The qPCR validation supported these findings by showing expression levels in AML patients. Because of WGCNA, we found pathways related to disease, such as mismatch repair, cell cycle regulation, and p53 signaling, that these coding RNAs might affect. Additionally, we figured out 20 genes closely linked to Linc01089 and Linc01578. We established a protein-protein interaction (PPI) network to gain a deeper understanding of their roles in AML. Conclusions: While proposing their involvement in cancer-causing pathways, our study emphasizes the reduction of Linc01089 and Linc01578 in AML cases. This discovery lays the groundwork for exploration into how these lncRNAs could serve as targets for interventions in AML. © 2025
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