ArticleMolecular cancer2015
Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression.
Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Perspectives of long non-coding RNAs in cancer.Molecular biology reports · 2017Pooled it
- Article
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- IKAROS Gene Regulatory Network Reveal ERG as a Vulnerability in B-cell Acute Lymphoblastic Leukemia.bioRxiv : the preprint server for biology · 2025Article
- Role of Non-coding RNAs in Acute Myeloid Leukemia.Non-coding RNA · 2025Review
- Functions, mechanisms, and therapeutic implications of noncoding RNA in acute myeloid leukemia.Fundamental research · 2025Review
- Long noncoding RNAs in acute myeloid leukemia: biomarkers, prognostic indicators, and treatment potential.Cancer cell international · 2025Review
- Immune checkpoints and ncRNAs: pioneering immunotherapy approaches for hematological malignancies.Cancer cell international · 2024Review
- The role of long noncoding RNAs in the diagnosis, prognosis and therapeutic biomarkers of acute myeloid leukemia.Annals of hematology · 2024Review
- Recent advances on biogenesis, functions and therapeutic potential of long noncoding RNAs in T cell acute lymphoblastic leukemia.Discover oncology · 2024Review
- Transcriptome free energy can serve as a dynamic patient-specific biomarker in acute myeloid leukemia.NPJ systems biology and applications · 2024Article
- KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST.Cell communication and signaling : CCS · 2024Review
- Novel lncRNAs LINC01221, RP11-472G21.2 and CRNDE are markers of differential expression in pediatric patients with T cell acute lymphoblastic leukemia.Cancer cell international · 2024Article
- HERV-K (HML-2) insertion polymorphisms in the 8q24.13 region and their potential etiological associations with acute myeloid leukemia.Archives of virology · 2023Article
- Anesthetic‑specific lncRNA and mRNA profile changes in blood during colorectal cancer resection: A prospective, matched‑case pilot study.Oncology reports · 2023Article
- The Promising Role of Non-Coding RNAs as Biomarkers and Therapeutic Targets for Leukemia.Genes · 2023Review
- Diagnostic and Therapeutic Implications of Long Non-Coding RNAs in Leukemia.Life (Basel, Switzerland) · 2022Review
- Non-coding RNAs: are they the protagonist or antagonist in the regulation of leukemia?American journal of translational research · 2022Review
- Long Noncoding RNA and Circular RNA: Two Rising Stars in Regulating Epithelial-Mesenchymal Transition of Pancreatic Cancer.Frontiers in oncology · 2022Review
- lncExplore: a database of pan-cancer analysis and systematic functional annotation for lncRNAs from RNA-sequencing data.Database : the journal of biological databases and curation · 2021Article
9 more citing papers are in PubMed but not listed here.
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6 authors.
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Abstract
backgroundAccumulating evidence suggests that some long noncoding RNAs (lncRNAs) are involved in certain diseases, such as cancer. The lncRNA, CCDC26, is related to childhood acute myeloid leukemia (AML) because its copy number is altered in AML patients.
resultsWe found that CCDC26 transcripts were abundant in the nuclear fraction of K562 human myeloid leukemia cells. To examine the function of CCDC26, gene knockdown (KD) was performed using short hairpin RNAs (shRNAs), and four KD clones, in which CCDC26 expression was suppressed to 1% of its normal level, were isolated. This down-regulation included suppression of CCDC26 intron-containing transcripts (the CCDC26 precursor mRNA), indicating that transcriptional gene suppression (TGS), not post-transcriptional suppression, was occurring. The shRNA targeting one of the two CCDC26 splice variants also suppressed the other splice variant, which is further evidence for TGS. Growth rates of KD clones were reduced compared with non-KD control cells in media containing normal or high serum concentrations. In contrast, enhanced growth rates in media containing much lower serum concentrations and increased survival periods after serum withdrawal were observed for KD clones. DNA microarray and quantitative polymerase chain reaction screening for differentially expressed genes between KD clones and non-KD control cells revealed significant up-regulation of the tyrosine kinase receptor, KIT, hyperactive mutations of which are often found in AML. Treatment of KD clones with ISCK03, a KIT-specific inhibitor, eliminated the increased survival of KD clones in the absence of serum.
conclusionsWe suggest that CCDC26 controls growth of myeloid leukemia cells through regulation of KIT expression. A KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered.
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