ArticleThe Journal of biological chemistry2012
The helicase HAGE expressed by malignant melanoma-initiating cells is required for tumor cell proliferation in vivo.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Comparative Transcriptomics Analyses Identify DDX43 as a Cellular Regulator Involved in Suppressing HSV-2 Replication.Viruses · 2025Article
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- Fine Mapping of the High-pH Tolerance and Growth Trait-Related Quantitative Trait Loci (QTLs) and Identification of the Candidate Genes in Pacific White Shrimp (Litopenaeus vannamei).Marine biotechnology (New York, N.Y.) · 2020Article
- Stem-Mesenchymal Signature Cell Genes Detected in Heterogeneous Circulating Melanoma Cells Correlate With Disease Stage in Melanoma Patients.Frontiers in molecular biosciences · 2020Article
- Therapeutic Strategies Targeting Cancer Stem Cells and Their Microenvironment.Frontiers in oncology · 2019Review
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- The DEAD-box protein DDX43 (HAGE) is a dual RNA-DNA helicase and has a K-homology domain required for full nucleic acid unwinding activity.The Journal of biological chemistry · 2017Article
- Identification of Predictive DNA Methylation Biomarkers for Chemotherapy Response in Colorectal Cancer.Frontiers in pharmacology · 2017Article
- Salmonella VNP20009-mediated RNA interference of ABCB5 moderated chemoresistance of melanoma stem cell and suppressed tumor growth more potently.Oncotarget · 2016Article
- ABCB5 maintains melanoma-initiating cells through a proinflammatory cytokine signaling circuit.Cancer research · 2014Article
- HAGE (DDX43) is a biomarker for poor prognosis and a predictor of chemotherapy response in breast cancer.British journal of cancer · 2014Article
- The helicase HAGE prevents interferon-α-induced PML expression in ABCB5+ malignant melanoma-initiating cells by promoting the expression of SOCS1.Cell death & disease · 2014Article
- Identification of a class of human cancer germline genes with transcriptional silencing refractory to the hypomethylating drug 5-aza-2'-deoxycytidine.Oncoscience · 2014Article
- Melanoma stem cells and metastasis: mimicking hematopoietic cell trafficking?Laboratory investigation; a journal of technical methods and pathology · 2014Review
- Molecular and cellular pathogenesis of melanoma initiation and progression.Cellular and molecular life sciences : CMLS · 2013Review
- Ras-mutant cancer cells display B-Raf binding to Ras that activates extracellular signal-regulated kinase and is inhibited by protein kinase A phosphorylation.The Journal of biological chemistry · 2013Article
- Genetically determined ABCB5 functionality correlates with pigmentation phenotype and melanoma risk.Biochemical and biophysical research communications · 2013Article
- The DEAD/DEAH box helicase, DDX11, is essential for the survival of advanced melanomas.Molecular cancer · 2012Article
- The KH domain facilitates the substrate specificity and unwinding processivity of DDX43 helicase.The Journal of biological chemistryArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant melanoma-initiating cells (MMIC) are a subpopulation of cells responsible for melanoma tumor growth and progression. They are defined by the expression of the ATP-binding cassette (ABC) subfamily B member 5 (ABCB5). Here, we identified a critical role for the DEAD-box helicase antigen (HAGE) in ABCB5+ MMIC-dependent tumorigenesis and show that HAGE-specific inactivation inhibits melanoma tumor growth mediated by this tumor-initiating population. Knockdown of HAGE led to a significant decrease in RAS protein expression with a concomitant decrease in activation of the AKT and ERK signaling pathways implicated to play an important role in melanoma progression. To confirm that the reduction in NRAS (Neuroblastoma RAS) expression was dependent on the HAGE helicase activity, we showed that NRAS, effectively silenced by siRNA, could be rescued by reintroduction of HAGE in cells lacking HAGE. Furthermore, we provide a mechanism by which HAGE promotes NRAS unwinding in vitro. We also observed using tumor transplantation in Non-obese diabetic/severe combined immunodeficiency mice that the HAGE knockdown in a ABCB5+ melanoma cell line displayed a significant decrease in tumor growth and compared with the control. Our results suggest that the helicase HAGE is required for ABCB5+ MMIC-dependent tumor growth through promoting RAS protein expression and that cancer therapies targeting HAGE helicase may have broad applications for treating malignant melanoma and potentially other cancer types.
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