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Long intergenic non-protein coding RNA 1123 (LINC01123) is a human long non-coding RNA gene located on chromosome 2q13 and is composed of four exons spanning over 8 kb[1][2][3]. LINC01123 functions as an oncogenic lncRNA. It regulates numerous cancer-related processes, including cell proliferation, apoptosis resistance, migration, invasion, stemness, epithelial-mesenchymal transition, metabolic reprogramming (preferentially glycolysis), and immune escape. Mechanistically, LINC01123 acts as a competing endogenous RNA (ceRNA) by sequestering key microRNAs, leading to derepression of oncogenes and facilitating malignant behaviors in tumor cells. It also forms complexes with specific proteins (e.g., SRSF7) to influence alternative splicing events relevant to cancer biology. High expression of LINC01123 is consistently associated with poor clinicopathological features and reduced survival in multiple solid tumors, leading to its consideration as both a prognostic biomarker and a potential therapeutic target in oncology. Additionally, its dysregulation is implicated in non-oncologic conditions such as atherosclerosis and thrombotic disease, although its major clinical relevance is in malignancies[2][3]. No drugs directly targeting LINC01123 have been clinically described, but its oncogenic functions and network of molecular interactions are actively studied as future therapeutic modalities[2][5][1].
Acts as a competing endogenous RNA (ceRNA), sequestering microRNAs (e.g., miR-34a-5p, miR-663a, miR-4766-5p, miR-625-5p, miR-516b-5p, miR-361-3p, miR-449b-5p), leading to upregulation of oncogenes (e.g., TUFT1, CMIP, PYCR1, LASP1, VEGFA, TSPAN1, Gli1, NOTCH1)[2][3][5]. Forms RNA-protein complexes (e.g., with SRSF7) to regulate pre-mRNA splicing and cancer-related gene expression[2]. Modulates key signaling pathways such as NOTCH and Hedgehog in cancer progression[2][5].
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