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Taurine upregulated gene 1 (TUG1) is a long non-coding RNA (lncRNA) that was originally identified as being essential for the development of photoreceptors in the retina [3, 10]. It functions as a critical regulator of gene expression through various mechanisms, most notably by acting as a competing endogenous RNA (ceRNA) that "sponges" microRNAs and by recruiting chromatin-modifying complexes like Polycomb Repressive Complex 2 (PRC2) to specific genomic loci [1, 7]. TUG1 is frequently overexpressed in a wide range of human malignancies, including hepatocellular carcinoma, colorectal cancer, and osteosarcoma, where it promotes cell proliferation, migration, and resistance to apoptosis [4, 6, 12]. Beyond oncology, TUG1 is implicated in the pathogenesis of liver fibrosis, diabetic nephropathy, and neurodegenerative conditions such as Alzheimer's disease [4, 11, 14]. Due to its pivotal role in disease progression and its presence in body fluids, TUG1 is being investigated as both a diagnostic biomarker and a therapeutic target [6, 7]. Experimental strategies to inhibit TUG1 primarily involve the use of antisense oligonucleotides (ASOs) to induce its degradation, which has shown promise in preclinical models for reducing tumor growth and restoring normal cellular function [13].
Knockdown of long non-coding RNA expression via antisense oligonucleotides to inhibit oncogenic signaling and restore microRNA regulatory networks
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