{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Recent studies have revealed that the long non‐coding RNA LINC01016 functions as a multifaceted regulator in hormone‐related cancers. In estrogen receptor–positive luminal breast cancer, LINC01016 has been identified as a direct transcriptional target of ERα and is implicated in modulating estrogen signaling, cell proliferation, and autophagy‐related pathways – thereby serving as a promising prognostic biomarker."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In endometrial cancer, LINC01016 is significantly upregulated and exerts oncogenic effects by acting as a competing endogenous RNA; it sequesters miR‑302a‑3p and miR‑3130‑3p to relieve suppression of NFYA, which in turn upregulates SATB1 and promotes malignant cellular behaviors."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " Detailed molecular characterization of LINC01016 further suggests that isoform variability and resultant conformational changes may influence its functional roles in cancer pathogenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " Moreover, altered expression of LINC01016 has been found to correlate with lymph node metastasis in thyroid carcinoma, indicating its potential involvement in tumor dissemination beyond breast and endometrial malignancies."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " Collectively, these findings underscore the emerging importance of LINC01016 as a critical mediator of hormone-driven oncogenic processes and as a potential target for diagnostic and therapeutic strategies across multiple cancer types.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Philip Jonsson, Cristian Coarfa, Fahmi Mesmar, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "LINC01016 promotes the malignant phenotype of endometrial cancer cells by regulating the miR-302a-3p/miR-3130-3p/NFYA/SATB1 axis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Death Dis (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41419-018-0291-9"}], "href": "https://doi.org/10.1038/s41419-018-0291-9"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29467441"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29467441"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Enrique I Ramos, Barbara Yang, Yasmin M Vasquez, et al. 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