{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nInitial studies in prostate cancer identified PRNCR1 as an overexpressed long non‐coding RNA that binds to the androgen receptor (AR) to enhance both ligand‐dependent and ligand‐independent AR‐mediated transcription and cell proliferation. These reports proposed that PRNCR1, by associating with chromatin modifiers and partnering with other lncRNAs, contributes to castration‐resistance and aggressive tumor behavior. However, subsequent comprehensive RNA‐sequencing and functional analyses have challenged its involvement in AR signaling and its prognostic value in prostate cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond the prostate, PRNCR1 has been implicated in a diverse range of malignancies. In colorectal cancer, for instance, overexpression of PRNCR1 promotes cell proliferation and influences cell cycle progression, with certain single nucleotide polymorphisms (SNPs) affecting its secondary structure and correlating with disease risk and tumor stage. In gastric cancer, specific PRNCR1 variants have been linked to altered susceptibility. Moreover, in non‐small cell lung cancer (NSCLC) and oral squamous cell carcinoma, PRNCR1 appears to act as a competing endogenous RNA (ceRNA), sponging microRNAs (e.g. miR‐448) to de‐repress oncogenic targets such as HEY2, while similar ceRNA mechanisms have been proposed in breast and ovarian cancers where PRNCR1 modulates signaling axes (for example, via miR‐377/CCND2 or miR‐653‑5p/ELF2). In addition, genetic association studies in lung cancer have also revealed links between PRNCR1 polymorphisms and cancer susceptibility."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "17"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic variations within the PRNCR1 locus seem to modulate its function and have been proposed as biomarkers for cancer risk across populations, as demonstrated by meta‐analyses and SNP association studies. Beyond oncogenesis, emerging evidence suggests that PRNCR1 may also play roles in non‐neoplastic conditions: it has been implicated in osteogenic differentiation and osteolysis, as well as in pulmonary vascular endothelial injury via regulation of inflammatory signaling cascades through interactions with microRNAs like miR‑330‑5p and subsequent modulation of targets such as TLR4. Comprehensive reviews further underscore the multifaceted regulatory roles of PRNCR1—not only as an oncogenic driver via miRNA sponging and chromatin remodeling but also as a potential target in diverse human disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "24"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Liuqing Yang, Chunru Lin, Chunyu Jin, et al. 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