{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long non‐coding RNA LINC00982 has emerged as an important regulatory molecule with context‐dependent functions. In several studies investigating gastric cancer, LINC00982 was found to be significantly downregulated in tumor tissues and gastric juice, and its reduced expression was correlated with enhanced cell proliferation, deeper invasion, advanced TNM stage, lymph node metastasis, and poorer patient survival. Overexpression of LINC00982 in gastric cancer cells inhibited proliferation, migration, and invasion through mechanisms that involve binding to transcription factors – for instance, by sequestering HEY1 to block its binding to the CTSF promoter – as well as modulating cell cycle regulators such as P15 and P16."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In renal cancer, decreased expression of LINC00982 has been reported, and its restoration led to inhibition of cell proliferation and promotion of apoptosis—effects that appear to be mediated, at least in part, via downregulation of PI3K/AKT signaling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " Similarly, in breast cancer and papillary thyroid carcinoma, low levels of LINC00982 are associated with aggressive tumor behavior and poor clinical outcomes. Functional studies in these cancers indicate that LINC00982 acts as a tumor suppressor by interfering with key signaling pathways such as STAT3/NF‑κB and by serving as a molecular sponge for oncogenic microRNAs, thereby modulating downstream targets that affect cell proliferation, migration, and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond oncological contexts, LINC00982 has also been implicated in non‑tumor conditions. In a model of myocardial ischemia/reperfusion injury, elevated LINC00982 levels were linked to increased apoptosis and inflammation in cardiomyocytes, whereas pharmacologic downregulation of LINC00982 (for example, via dexmedetomidine treatment) promoted cell survival through activation of the PI3K/AKT pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Moreover, in the context of Epstein–Barr virus–associated malignancies, LINC00982 is among host long non‐coding RNAs modulated by viral factors, suggesting that its regulatory network may extend to virus‐induced tumorigenesis, although its precise functional role in this setting requires further elucidation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In summary, current evidence indicates that LINC00982 functions predominantly as a tumor suppressor in several cancer types by modulating key transcription factors, signaling pathways, and cell cycle regulators. Its downregulation correlates with enhanced tumor progression and poorer clinical outcomes, while its restoration holds therapeutic promise. Conversely, in specific non‐cancerous contexts such as myocardial injury, LINC00982 appears to facilitate deleterious cellular responses. These multifaceted roles underscore the potential of LINC00982 both as a prognostic biomarker and as a target for novel therapeutic strategies.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lei Zheng, Junlin Cao, Lijie Liu, et al. 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