{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nIn hepatocellular carcinoma (HCC), the long noncoding RNA NPSR1‐AS1 acts as a hypoxia‐responsive regulator. Under low oxygen levels, HIF‑1α induces its expression, which in turn promotes HCC cell proliferation and glycolysis. Mechanistically, elevated NPSR1‐AS1 levels enhance the phosphorylation of ERK1/2 and increase pyruvate kinase M2 (PKM2) expression, thereby activating the MAPK/ERK pathway. Consequently, silencing NPSR1‐AS1 blunts hypoxia‐induced pathway activation and metabolic reprogramming, reducing tumor cell proliferation and glycolysis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "<br><br>\n\nIn thyroid cancer (TC), NPSR1‐AS1 is also highly expressed and contributes to tumor progression by modulating its neighboring gene, NPSR1. Functioning in concert with the RNA‐binding protein ELAVL1, NPSR1‐AS1 stabilizes NPSR1 mRNA, which in turn activates the MAPK pathway. This lncRNA–RBP–mRNA interaction supports enhanced proliferation, colony formation, and migration of TC cells, underscoring its role in the malignant phenotype"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "<br><br>\n\nTogether, these findings suggest that NPSR1‐AS1 operates as an oncogenic lncRNA across different tumor types by engaging key signaling cascades such as the MAPK/ERK pathway. In both HCC and TC, its regulation of cellular metabolism and proliferation underlines the potential of targeting the NPSR1‐AS1 axis as a novel therapeutic strategy."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Haibin He, Tianxiang Chen, Huanye Mo, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Hypoxia-inducible long noncoding RNA NPSR1-AS1 promotes the proliferation and glycolysis of hepatocellular carcinoma cells by regulating the MAPK/ERK pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochem Biophys Res Commun (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.bbrc.2020.09.076"}], "href": "https://doi.org/10.1016/j.bbrc.2020.09.076"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "33008585"}], "href": "https://pubmed.ncbi.nlm.nih.gov/33008585"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Tiangen Ni, Dan Guo, Ling Tan, et al. "}, {"type": "b", "children": [{"type": "t", "text": "NPSR1-AS1 activates the MAPK pathway to facilitate thyroid cancer cell malignant behaviors via recruiting ELAVL1 to stabilize NPSR1 mRNA."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Cycle (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1080/15384101.2021.1979773"}], "href": "https://doi.org/10.1080/15384101.2021.1979773"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "35030041"}], "href": "https://pubmed.ncbi.nlm.nih.gov/35030041"}]}]}]}