{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC16A1‐AS1 is emerging as an important regulator of cancer cell proliferation and cell cycle progression, although its expression and function appear to be context‐dependent. In oral squamous cell carcinoma (OSCC), one study reported that SLC16A1‐AS1 is highly expressed and promotes proliferation through cell‐cycle regulation (via cyclin D1) and enhanced clonogenicity, whereas another investigation in OSCC revealed that its overexpression inhibits the maturation of an oncogenic miRNA (miR-5088-5p), thereby suppressing cell proliferation. In triple-negative breast cancer (TNBC), differential reports describe either downregulation of SLC16A1‐AS1 from large-scale analyses or upregulation associated with increased cell proliferation, invasion, and reduced apoptosis; such discrepancies highlight the context‐specific regulatory role of this lncRNA across various tumor types."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nA second key mechanism by which SLC16A1‐AS1 influences tumor progression is through the regulation of microRNA (miRNA) maturation. In glioblastoma, SLC16A1‐AS1 interacts directly with premature miR-1269, inhibiting its maturation and thereby favoring oncogenic proliferation, migration, and invasion. Similarly, in TNBC, an inverse relationship was observed between SLC16A1‐AS1 and miR-526b levels, suggesting that this lncRNA modulates cell survival and apoptotic pathways via miRNA interactions. In addition, the direct binding of SLC16A1‐AS1 with premature miR-5088-5p in OSCC underscores its role as a molecular sponge or processing regulator, ultimately impacting cell proliferation dynamics."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}, {"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, SLC16A1‐AS1 participates in modulating the tumor microenvironment, particularly in hepatocellular carcinoma (HCC). Exosome‐derived SLC16A1‐AS1 from HCC cells has been shown to induce M2-type macrophage polarization by enhancing the stabilization of SLC16A1 mRNA through facilitating its interaction with HNRNPA1. This process increases lactate influx and activates downstream c-Raf/ERK signaling, while reciprocal IL-6 secretion by M2 macrophages further boosts SLC16A1‐AS1 stabilization via m6A methylation, collectively promoting tumor proliferation, invasion, and glycolysis. Parallel work has explored its broader molecular mechanisms in HCC tumorigenesis, underscoring its potential as both a diagnostic biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Hao Feng, Xiaoqi Zhang, Wenli Lai, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "LncRNA SLC16A1-AS1 regulates the miR-182/PDCD4 axis and inhibits the triple-negative breast cancer cell cycle."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Immunopharmacol Immunotoxicol (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1080/08923973.2022.2056482"}], "href": "https://doi.org/10.1080/08923973.2022.2056482"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "35316129"}], "href": "https://pubmed.ncbi.nlm.nih.gov/35316129"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Tiecheng Li, Di Wang, Shuo Yang "}, {"type": "b", "children": [{"type": "t", "text": "Analysis of the subcellular location of lncRNA SLC16A1-AS1 and its interaction with premature miR-5088-5p in oral squamous cell carcinoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Odontology (2023)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s10266-022-00712-w"}], "href": "https://doi.org/10.1007/s10266-022-00712-w"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "35829849"}], "href": "https://pubmed.ncbi.nlm.nih.gov/35829849"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Xingjuan Zhao, Lei Fu, Liqin Zhai, et al. 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