{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long noncoding RNA CCDC26 has emerged as a multifunctional regulatory molecule with context‐dependent roles in tumorigenesis. In acute myeloid leukemia, CCDC26 expression is frequently altered, and experimental knockdown in myeloid leukemia cells leads to diminished growth under normal conditions but enhanced survival under serum‐limited conditions through upregulation of the tyrosine kinase receptor KIT, suggesting that CCDC26 can modulate cellular proliferation and survival via KIT‐dependent pathways."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In gliomas, CCDC26 is frequently overexpressed relative to normal brain tissue; its silencing in glioma cell lines reduces cell proliferation, migration, and invasion while promoting apoptosis. This effect appears to be mediated, at least in part, by modulation of microRNA expression (for example, upregulation of miR‐203 following CCDC26 knockdown), supporting an oncogenic role in glioma progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " Furthermore, genetic studies have identified polymorphisms within the CCDC26 region as risk factors for glioma and pediatric brain tumors, indicating that both altered transcript levels and inherited sequence variation in CCDC26 contribute to brain tumor susceptibility."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In leukemia, beyond its role in controlling cell growth via KIT, CCDC26 has also been implicated in cellular differentiation. Knockdown studies in K562 cells indicate that reduced CCDC26 expression alters globin gene transcription during hemin‐induced erythroid differentiation – leading to upregulation of embryonic globins and suppression of adult globins – with transcriptional modulators such as FOG‑2 emerging as potential mediators of this effect."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " Additionally, ceRNA networks involving CCDC26 have been linked to drug resistance in leukemia cells, where perturbation of CCDC26 alters the expression of key regulators through microRNA sponging mechanisms."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In thyroid cancer, CCDC26 is similarly upregulated and functions as an oncogenic lncRNA. Mechanistic studies demonstrate that CCDC26 can bind and sequester miR‑422a, thereby de‐repressing downstream targets such as EZH2 and Sirt6, which in turn enhances proliferation, invasion, and survival of thyroid cancer cells both in vitro and in vivo."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these studies reveal that CCDC26 functions as a key regulatory hub in various cancer types – modulating cell growth, survival, differentiation, and chemoresistance – predominantly by acting through microRNA interactions and influencing downstream oncogenic signaling pathways. Such multifunctionality underscores its potential as both a biomarker for tumor susceptibility and a candidate therapeutic target.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Tetsuo Hirano, Ryoko Yoshikawa, Hironori Harada, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Cancer (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1186/s12943-015-0364-7"}], "href": "https://doi.org/10.1186/s12943-015-0364-7"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25928165"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25928165"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Shilei Wang, Yuzuo Hui, Xiaoming Li, et al. 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