Plaque enriched long noncoding RNA in atherosclerotic and inflammatory bowel macrophage regulation (PELATON)

PELATON (Plaque enriched long noncoding RNA in atherosclerotic and inflammatory bowel macrophage regulation) is a nuclear-expressed, monocyte- and macrophage-specific long noncoding RNA (lncRNA), originally identified as LINC01272, and also known by several aliases including GCRL1 and SMIM25[1][2]. It is highly expressed in regions of unstable atherosclerotic plaque and in inflammatory macrophages, as well as in several cancers including glioblastoma, colorectal, gastric, and lung cancer[1][2]. PELATON regulates critical macrophage functions such as phagocytosis, lipid uptake, and ROS production and is required for proper oxidative LDL uptake via control of CD36. In cancer, particularly glioblastoma, PELATON acts as a ferroptosis suppressor mainly via a mutant p53-mediated pathway, promoting cancer cell proliferation and resistance to cell death. Knockdown or suppression of PELATON decreases phagocytosis, enhances sensitivity to ferroptosis inducers, and inhibits tumor cell invasion and proliferation. PELATON expression is associated with poor prognosis and it may serve as both a disease biomarker and a potential therapeutic target, though no approved therapies currently target this lncRNA[1][2].

Other names

GCRL1GC-related lncRNA1LINC01272SMIM25long intergenic non-protein coding RNA 1272small integral membrane protein 25

Acts as an lncRNA decoy/sponge to regulate target miRNAs and genes; Suppresses ferroptosis, particularly by modulating ROS and iron metabolism in GBM via mutant p53 pathway[2]; Inhibits CD36 expression, reducing oxLDL uptake in macrophages[1]; Modulates expression of BACH1, CD44, SLC7A11, ACSL4, and COX2[2]