{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nDUXAP10 is a pseudogene‐derived long non‐coding RNA that is consistently overexpressed in a variety of cancers and other pathological contexts. In colorectal cancer, for example, its up‐regulation correlates with advanced pathological stage, larger tumor size, and lymph node metastasis, while in other malignancies such as bladder cancer, gastric cancer, chronic myelogenous leukemia, hepatocellular carcinoma, papillary thyroid carcinoma, renal cell carcinoma, glioma, and osteosarcoma, DUXAP10 overexpression is similarly associated with aggressive disease features. Moreover, its aberrant expression has also been implicated in age‐related dysfunction of adipose stem cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n\nIn mechanistic studies, DUXAP10 exerts its oncogenic effects by modulating critical cellular processes. In colorectal cancer, DUXAP10 binds to lysine‐specific demethylase 1 (LSD1) to silence the tumor suppressors p21 and PTEN, thereby promoting cell proliferation and inhibiting apoptosis. In bladder cancer and papillary thyroid carcinoma, its knockdown leads to cell cycle arrest and apoptosis, partly by inhibiting the PI3K/Akt/mTOR pathway. In hepatocellular carcinoma, DUXAP10 contributes to both cell proliferation and epithelial–mesenchymal transition (EMT), with one study demonstrating that its silencing reduces β‑catenin and phosphorylated Akt levels, while another report shows that DUXAP10 negatively regulates miR‑1914, thereby modulating the downstream GPR39/PI3K/Akt/mTOR signaling axis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}, {"type": "fg_fs", "start_ref": "5", "end_ref": "7"}]}, {"type": "t", "text": "\n\nBeyond proliferation and survival, DUXAP10 also modulates the stemness properties of tumor cells. In glioma, knockdown of DUXAP10 reduces the expression of stemness markers and tumor sphere-forming ability by interacting with the RNA-binding protein HuR to prevent its nuclear translocation, which in turn stabilizes Sox12 mRNA in the cytoplasm. Similarly, in osteosarcoma, DUXAP10 enhances cell proliferation, migration, and invasion by binding HuR to increase the stability of SOX18 mRNA."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n\nIn addition to its role in malignant processes, DUXAP10 contributes to age-related cellular dysfunction. In aged adipose stem cells, accumulation of DUXAP10 acts as a decoy for miR‑214‑3p, resulting in the upregulation of RASSF5 and leading to impaired proliferation, reduced migration, and increased cellular senescence. Targeting DUXAP10 in these cells has been shown to rejuvenate their regenerative potential, suggesting a novel therapeutic avenue for age-associated tissue repair."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "\n\nCollectively, studies across a spectrum of cancers and in stem cell aging underscore the multifaceted oncogenic and regulatory roles of DUXAP10. Its involvement in key signaling pathways, including PI3K/Akt/mTOR and Wnt/β‑catenin, as well as its modulation of RNA-binding proteins and microRNAs, positions DUXAP10 as both a potential biomarker and a promising therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yifan Lian, Yetao Xu, Chuanxing Xiao, et al. 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