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MicroRNA-155 is a small, non-coding RNA molecule (microRNA) highly conserved among vertebrates, encoded by the MIR155 host gene (MIR155HG), originally called the B-cell Integration Cluster (BIC)[1][5][8]. It is a master regulator of gene expression at the post-transcriptional level, primarily by binding to complementary sequences in target messenger RNAs to inhibit their expression or induce degradation. MiR-155 plays essential roles in immune system development and function, controlling the differentiation, proliferation, and activation of diverse immune cells such as B cells, T cells (including Th1, Th2, Th17, and Tregs), macrophages, dendritic cells, and invariant natural killer T cells[2][3][4][6]. Its expression is dynamically regulated in response to inflammatory cues, cytokines, or pathogen exposure[4][5][8]. Pathologically, miR-155 is frequently overexpressed in cancers (notably lymphoid malignancies), where it drives tumorigenesis and supports malignant cell survival[7][9]. It is also involved in autoimmune and inflammatory diseases, cardiovascular pathologies, and infections, making it a prominent therapeutic target for drug development[5][7]. Experimental drugs targeting miR-155 mostly involve antisense technologies delivered via nanoparticles, aiming to knock down excess miR-155 and restore normal cellular function in disease, though clinical translation remains challenging due to safety and specificity concerns[7]. MiR-155 is commonly measured as a biomarker for disease diagnosis and monitoring, especially in cancer and autoimmune conditions, reflecting its pathological importance. However, therapeutic targeting must balance efficacy with the risk of impairing essential immune functions and hematopoiesis, a major challenge for future clinical applications[5][7].
Inhibition of miR-155 function by antisense oligonucleotides (anti-miR-155) Suppression of pathological overexpression, restoring normal gene regulation[7]
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