{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long non‐coding RNA LINC00899 has emerged as a multifunctional regulator with context‐dependent roles in several human diseases. In cervical cancer, LINC00899 is downregulated, and its overexpression suppresses cell viability, proliferation, migration, and invasion by acting as a competing endogenous RNA (ceRNA) that sponges miR‐944, thereby upregulating ESR1 and counteracting epithelial–mesenchymal transition (1). In breast cancer, decreased LINC00899 levels correlate with poorer relapse‐free survival, whereas its enforced expression inhibits tumor cell growth and metastasis via the miR‐425/DICER1 axis; in addition, ceRNA network analyses in hypoxic conditions further implicate LINC00899 in modulating key signaling molecules (6,9). In spinal ependymoma, LINC00899 is upregulated and promotes oncogenic properties by repressing the tumor suppressor RBL2 and modulating the FoxO pathway, with knockdown leading to increased RBL2, p21, p27, and Bax levels and consequent reduction in proliferation, migration, and invasion (7). In acute myeloid leukemia (AML), elevated LINC00899 expression is associated with poor prognosis, as it promotes cell proliferation and inhibits apoptosis by sponging miR‐744‐3p, which in turn results in the derepression of the transcription factor YY1; moreover, serum LINC00899 levels have been proposed as a noninvasive diagnostic and prognostic biomarker in this disease (5,8). Beyond oncology, LINC00899 facilitates osteogenic differentiation of human bone mesenchymal stem cells and may help prevent osteoporosis through binding miR‐374a to upregulate RUNX2 expression (2). Furthermore, in the context of cell cycle regulation, depletion of the chromatin‐associated form of LINC00899 leads to transcriptional upregulation of the neuronal microtubule‐binding protein TPPP/p25, thereby altering microtubule dynamics and inducing a robust mitotic delay (4). Collectively, these studies highlight that LINC00899 exerts critical regulatory functions through miRNA sponging and ceRNA mechanisms that impact tumorigenesis, differentiation, and mitotic progression (1,2,4,5,6,7,8,9).\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n "}, {"type": "b", "children": [{"type": "t", "text": "Citations:"}]}, {"type": "t", "text": "\n <br>\n (1)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ",\n (2)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ",\n (4)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ",\n (5)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ",\n (6)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ",\n (7)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ",\n (8)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ",\n (9)."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yu Chen, Yingjie Gu, Yanfang Gu, et al. 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