ArticleOncogene2018
Arresting of miR-186 and releasing of H19 by DDX43 facilitate tumorigenesis and CML progression.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Evaluation of obstructive sleep apnea: an analysis based on aberrant genes.Sleep & breathing = Schlaf & Atmung · 2023Article
- Abnormal regulation of miR-29b-ID1 signaling is involved in the process of decitabine resistance in leukemia cells.Cell cycle (Georgetown, Tex.) · 2023Article
- A comprehensive genome-wide analysis of long non-coding RNA and mRNA expression profiles of JAK2V617F-positive classical myeloproliferative neoplasms.Bioengineered · 2021Article
- Role and Clinical Utility of Cancer/Testis Antigens in Head and Neck Squamous Cell Carcinoma.Cancers · 2021Review
- Genome-wide methylation sequencing identifies progression-related epigenetic drivers in myelodysplastic syndromes.Cell death & disease · 2020Article
- Identification and validation of prognosis-related DLX5 methylation as an epigenetic driver in myeloid neoplasms.Clinical and translational medicine · 2020Article
- The Identification of Long Non-coding RNA H19 Target and Its Function in Chronic Myeloid Leukemia.Molecular therapy. Nucleic acids · 2020Article
- The Dual Role of miR-186 in Cancers: Oncomir Battling With Tumor Suppressor miRNA.Frontiers in oncology · 2020Review
- Article
- BCL2 overexpression: clinical implication and biological insights in acute myeloid leukemia.Diagnostic pathology · 2019Article
- Article
- Establishment and molecular characterization of decitabine-resistant K562 cells.Journal of cellular and molecular medicine · 2019Article
- MicroRNA-186 promotes cell proliferation and inhibits cell apoptosis in cutaneous squamous cell carcinoma by targeting RETREG1.Experimental and therapeutic medicine · 2019Article
- Long non-coding RNA H19 confers 5-Fu resistance in colorectal cancer by promoting SIRT1-mediated autophagy.Cell death & disease · 2018Article
- Article
- The KH domain facilitates the substrate specificity and unwinding processivity of DDX43 helicase.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-testis (CT) antigens, rarely in normal tissues except testis, are expressed in many tumor types. In recent years, DDX43 has been shown to be expressed in several malignancies. However, the role of DDX43 during tumorigenesis is not well established. In the present study, we explored the function of DDX43 in chronic myeloid leukemia (CML). We found that DDX43 overexpression in CML cell lines enhanced survival and colony formation, inhibited cell apoptosis, promoted tumorigenesis, and CML progression. In contrast, silencing of DDX43 inhibited cell survival and tumorigenesis. Upregulated H19 and downregulated miR-186 were identified in DDX43-transfected cells. Furthermore, we demonstrated that miR-186 targeted DDX43, and overexpressed miR-186 increased apoptosis and decreased cell survival. We also showed that DDX43 regulated the expression of H19 through demethylation and silencing H19 inhibited cell survival. Taken together, these results indicate that DDX43 provides critical support to the progression of CML by enhancing cell survival, colony formation, and inhibiting cell apoptosis, thereby implicating DDX43 as a potential therapeutic target in CML.
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