{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe microRNA let‐7g plays a critical role in its own biogenesis and maturation. Structural and binding studies have shown that let‐7g precursors are selectively recognized by the RNA‐binding proteins Lin28 and Lin28B through defined motifs in the terminal loop, which in turn block its processing by Dicer. These insights into the molecular contacts—including the zinc knuckle domains of Lin28—establish a paradigm for the negative regulation of let‐7g maturation, thereby controlling its availability in the cell."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn several cancer models, let‐7g has been shown to function largely as a tumor suppressor. For instance, in breast and hepatocellular carcinomas, its downregulation enables the up‐regulation of oncogenic drivers—including METTL3, KRAS, HMGA2, and IGF‐1R—thereby promoting epithelial–mesenchymal transition, proliferation, and metastasis. Moreover, in certain contexts such as HBV‐associated HCC, viral transcripts sequester let‐7g, de‐repressing its targets and contributing to oncogenesis, while in lung and nasopharyngeal carcinomas, restoration of let‐7g levels limits tumor cell viability and invasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "14"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nLet‐7g also modulates cellular responses to therapy and drug resistance in cancer. In ovarian and esophageal carcinomas, for example, enforced expression of let‐7g targets mediators of multidrug resistance such as IMP‐1 and ABCC10, thereby destabilizing downstream effectors like MDR1. In parallel, by suppressing NF‐κB1, let‐7g can enhance the sensitivity of lung cancer cells to ionizing radiation. Taken together, these observations highlight let‐7g as a potential therapeutic agent to overcome treatment resistance in diverse tumor models."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "20"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer, let‐7g has emerged as an important regulator within the cardiovascular system and metabolic settings. In vascular smooth muscle and endothelial cells, let‐7g directly targets the mRNA encoding LOX‐1, a receptor for oxidized LDL, thereby diminishing oxLDL uptake, oxidative stress, and apoptosis. These actions contribute to anti‐atherosclerotic and anti‐aging effects, and alterations in let‐7g levels in serum have been associated with metabolic syndrome and cardiovascular dysfunction."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "25"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies have expanded the functional landscape of let‐7g to include roles in immune regulation, developmental processes, and as a promising biomarker in diverse pathologies. Its altered expression has been implicated in shaping the profiles of circulating microRNAs in colorectal cancer, rheumatoid arthritis, and even Alzheimer’s disease. Furthermore, modulation of let‐7g through methylation changes has been linked to neural tube defects, while in infectious and inflammatory settings—such as tuberculosis and cholangiocarcinoma—competitive sponging by long noncoding RNAs results in altered expression of downstream oncogenic targets. These multifaceted activities underscore the potential of let‐7g not only as an indicator of disease progression but also as a therapeutic target across a wide array of conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "38"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Elena Piskounova, Srinivas R Viswanathan, Maja Janas, et al. 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