{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long non‐coding RNA CASC11 has emerged as an important regulator in a variety of human diseases, most notably in cancer. Multiple independent studies have demonstrated that CASC11 is upregulated in several malignancies—including colorectal cancer, hepatocellular carcinoma, lung cancer (both small cell and non‐small cell subtypes), glioma, ovarian carcinoma, and neuroblastoma—and acts as an oncogene by promoting key malignant features such as cell proliferation, migration, invasion, epithelial–mesenchymal transition, and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Mechanistically, CASC11 frequently exerts its oncogenic function through “sponging” tumor‐suppressive microRNAs—such as miR‑646, miR‑381‑3p, miR‑302, miR‑498, miR‑188‑5p, miR‑150, and miR‑676‑3p—which in turn leads to the de-repression of targets like RAB11FIP2, CDK1, FOXO3, and NOL4L."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "11"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In addition, CASC11 has been shown to interact with regulatory proteins such as hnRNP‑K, EZH2, and EIF4A3, thereby modulating key signaling pathways—including Wnt/β‑catenin, TGF‑β, and the PI3K/AKT/mTOR cascade—and influencing cell cycle progression via regulators like CDK1."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "14"}]}, {"type": "t", "text": " Moreover, transcription factors including c‑Myc, STAT3, SP1, and YY1 have been implicated in upregulating CASC11 expression, suggesting a complex regulatory loop that reinforces its oncogenic activities."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Notably, while CASC11 predominantly promotes tumor progression, it may also play contrasting roles in non‐malignant pathologies. For example, in atherosclerosis, CASC11 is downregulated and appears to exert protective effects by inhibiting IL‑9 and modulating vascular smooth muscle cell proliferation and apoptosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": " In postmenopausal osteoporosis, increased CASC11 correlates with elevated TNF‑α levels and is linked to prolonged treatment courses and higher recurrence rates."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Overall, the cumulative evidence indicates that CASC11 functions as a multifaceted regulator whose aberrant expression contributes to malignant progression by acting as a competing endogenous RNA, interacting with protein partners, and modulating several oncogenic signaling pathways. These features render CASC11 a promising diagnostic biomarker and a potential therapeutic target in diverse human cancers.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zheying Zhang, Chang Zhou, Yaya Chang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long non-coding RNA CASC11 interacts with hnRNP-K and activates the WNT/β-catenin pathway to promote growth and metastasis in colorectal cancer."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cancer Lett (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.canlet.2016.03.022"}], "href": "https://doi.org/10.1016/j.canlet.2016.03.022"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "27012187"}], "href": "https://pubmed.ncbi.nlm.nih.gov/27012187"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Huarong Luo, Chengdang Xu, Wei Le, et al. 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