ArticleInternational journal of hematology2012
Acute myeloid leukemia with t(7;21)(q11.2;q22) expresses a novel, reversed-sequence RUNX1-DTX2 chimera.
Article in International journal of hematology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 11 citations in OpenAlex.
- DTX3 inhibits cell migration, invasion, and epithelial-mesenchymal transition in colorectal cancer through the AKT signaling pathway.Translational cancer research · 2025Article
- [High expression of DTX2 promotes proliferation, invasion and epithelial-mesenchymal transition of oxaliplatin-resistant colorectal cancer cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- The DTX Protein Family:Cells · 2023Review
- [DTX2 overexpression promotes migration and invasion of colorectal cancer cells through the Notch2/Akt axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Elevated RUNX1 is a prognostic biomarker for human head and neck squamous cell carcinoma.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Inhibition of RFX6 Suppresses the Invasive Ability of Tumor Cells Through the Notch Pathway and Affects Tumor Immunity in Hepatocellular Carcinoma.Frontiers in oncology · 2021Article
- Article
- Neoplasia-associated Chromosome Translocations Resulting in Gene Truncation.Cancer genomics & proteomicsReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RUNX1 gene is frequently rearranged in acute leukemia. We cloned a novel RUNX1 chimeric gene generated by t(7;21)(q11.2;q22) in a patient with acute myeloid leukemia. 3'-rapid amplification of cDNA ends analysis showed a tail-to-tail fusion between RUNX1 on 21q22 and DTX2 on 7q11.2, with an insertion of short complementary sequence from UPK3B adjacent to DTX2. DTX2 encodes a putative E3-ubiquitin ligase with no known biological function. There are two possible functions of RUNX1-reversed UPK3B-DTX2: one from aberrant RUNX1 chimeric protein and the other from the reversed sequence of DTX2. The predicted aberrant protein expressed under the RUNX1 promoter was highly structurally similar to RUNX1a. In a reporter assay, the aberrant protein inhibited the trans-activation function of RUNX1 in a dominant-negative manner, similar to RUNX1a. In contrast, the DTX2 reversed sequence may degrade wild-type DTX2 transcript or suppress its translation. In conclusion, we identified a novel fusion RUNX1 partner, DTX2, which chimerize in a reverse direction. This is the first example of RUNX1 chimera in an opposing direction generated by chromosomal translocation in leukemia. In addition to the aberrantly truncated RUNX1 protein, the DTX2 antisense sequence may play some role in the development of leukemia carrying the t(7;21) translocation.
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