{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nDRAIC is a long noncoding RNA with multifaceted functions in cancer that vary depending on cellular context and tumor type. In prostate cancer, DRAIC is notably downregulated in advanced, castration‐resistant cases, and its decreased expression correlates with poor patient prognosis. Mechanistically, DRAIC binds to components of the IκB kinase complex to inhibit IκBα phosphorylation and NF‑κB activation, thereby suppressing cell invasion and anchorage‐independent growth. In parallel, high-throughput screening in breast cancer cells revealed that DRAIC regulates autophagic flux, although its pro-proliferative effects appear to be independent of autophagy."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nIn other tumor types, DRAIC participates in competing endogenous RNA (ceRNA) networks that modulate critical oncogenic pathways. In nasopharyngeal carcinoma, DRAIC is upregulated and functions by sponging miR‑122 to enhance SATB1 expression, thereby promoting cell growth, migration, and invasion. Conversely, studies in gastric cancer and certain breast cancer subtypes indicate lower expression of DRAIC, consistent with its tumor‐suppressive role in these contexts. In breast cancer, for example, DRAIC has been shown to sponge miR‑432‑5p to positively regulate SLBP and promote malignant behaviors, whereas in triple‐negative breast cancer ectopic DRAIC expression suppresses angiogenesis and metastasis via interaction with the tumor‐suppressor protein RBM47. Moreover, in lung adenocarcinoma, DRAIC is highly expressed and appears to facilitate proliferation, migration, and invasion by targeting miRNAs such as let‑7i‑5p."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "7"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies highlight DRAIC’s integration into broader regulatory networks in various cancers. For instance, investigations in esophageal cancer suggest that DRAIC, through a miR‑149‑5p/NFIB axis, modulates autophagy and cell behavior, while research in glioma points to a regulatory relationship between DRAIC and the epigenetic factor SET7/9 that may influence metastasis. Analyses of luminal breast cancer subtypes further underscore the importance of ceRNA interactions involving DRAIC. Collectively, these findings demonstrate that DRAIC is a context-dependent regulator of cancer progression, acting either as a tumor suppressor or an oncogene by modulating key signaling pathways, miRNA networks, and autophagic processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "10"}]}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Imke Tiessen, Marie H Abildgaard, Michal Lubas, et al. 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