{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMSC‐AS1 is a long non‑coding RNA that functions primarily as a competitive endogenous RNA (ceRNA) to modulate the expression of key regulatory proteins. In bone tissue, for example, MSC‑AS1 has been shown to promote the osteogenic differentiation of bone marrow‑derived mesenchymal stem cells by sponging microRNA‑140‑5p, thereby up‐regulating BMP2 and potentially alleviating osteoporosis. In pancreatic ductal adenocarcinoma, an elevated MSC‑AS1 level similarly acts as a ceRNA, sequestering microRNA‑29b‑3p to derepress the oncogene CDK14, which in turn enhances cell proliferation and diminishes gemcitabine‑induced apoptosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn several other malignancies, MSC‑AS1 plays an oncogenic role by modulating distinct microRNAs and their target genes. In kidney renal clear cell carcinoma, it down‑regulates miR‑3924 to elevate WNT5A expression and activate the Wnt/β‑catenin signaling pathway, thereby fostering cell proliferation and migration. In temozolomide‑resistant glioma, MSC‑AS1 sponges miR‑373‑3p to enhance CPEB4 levels and activate PI3K/Akt signaling, contributing to chemoresistance. Similarly, in osteosarcoma, MSC‑AS1 binding to miR‑142 leads to increased CDK6 expression and PI3K/Akt pathway activation, promoting tumor cell growth and decreasing cisplatin sensitivity. In gastric cancer, MSC‑AS1 supports aggressive cellular behavior via two mechanisms: by sustaining PFKFB3 expression to boost glycolysis and proliferation, as well as by down‑regulating miR‑142‑5p to influence DDX5 levels and inflammatory mediator secretion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies expand the oncogenic spectrum of MSC‑AS1. In lung adenocarcinoma, MSC‑AS1 facilitates tumor growth by sponging miR‑33b‑5p, which leads to increased expression of GPAM. It is also implicated in hepatocellular carcinoma, where its aberrant expression affects cell proliferation, migration, and apoptosis. A separate investigation into bladder carcinogenesis examined hypermethylated lncRNAs, including MSC‑AS1, pointing toward its potential epigenetic involvement in tumor initiation. Moreover, in melanoma, MSC‑AS1 promotes proliferation and glutaminolysis by binding to miR‑330‑3p to up‑regulate YAP1, thereby linking metabolic reprogramming with tumor progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Naidong Zhang, Xinyu Hu, Shuanghua He, et al. 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