ArticleCell death & disease2018
CUEDC2, a novel interacting partner of the SOCS1 protein, plays important roles in the leukaemogenesis of acute myeloid leukaemia.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- CUE domain-containing 2 promotes diffuse large B-cell lymphoma progression via PP2A-B55β degradation and shapes macrophage-mediated immune responses.Molecular biomedicine · 2026Article
- SOCS1 Protects Acute Myeloid Leukemia against Allogeneic T Cell-Mediated Cytotoxicity.Blood cancer discovery · 2025Article
- miRNA-7145-cuedc2 axis controls hematopoiesis through JAK1/STAT3 signaling pathway.Cell death discovery · 2024Article
- Rapid Remission With Upadacitinib in a Child With Refractory Crohn's Disease andCurrent therapeutic research, clinical and experimental · 2024Article
- Lysine deserts and cullin-RING ligase receptors: Navigating untrodden paths in proteostasis.iScience · 2023Article
- Article
- KIAA0317 regulates SOCS1 stability to ameliorate colonic inflammation.The FEBS journal · 2023Article
- CUEDC2 Drives β-Catenin Nuclear Translocation and Promotes Triple-Negative Breast Cancer Tumorigenesis.Cells · 2022Article
- Comprehensive analysis for cellular senescence-related immunogenic characteristics and immunotherapy prediction of acute myeloid leukemia.Frontiers in pharmacology · 2022Article
- The Emerging Role of Suppressors of Cytokine Signaling (SOCS) in the Development and Progression of Leukemia.Cancers · 2021Review
- MDMX Recruits UbcH5c to Facilitate MDM2 E3 Ligase Activity and Subsequent p53 DegradationCancer research · 2021Article
- Article
- SOCS1 and its Potential Clinical Role in Tumor.Pathology oncology research : POR · 2019Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Downregulation of suppressor of cytokine signalling-1 (SOCS1) is one of the vital reasons for JAK1-STAT3 pathway activation in acute myeloid leukaemia (AML). CUE domain-containing 2 (CUEDC2) was a novel interacting partner of SOCS1 and a positive correlation between the expression of CUEDC2 and SOCS1 was confirmed in primary AML cells and AML cell lines without SOCS1 promoter methylation. We aimed to explore roles of CUEDC2 in regulating ubiquitin-mediated degradation of SOCS1 in the leukaemogenesis of AML.According to in vitro experiments, CUEDC2 overexpression increased the level of SOCS1 protein, suppressed JAK1-STAT3 pathway activation. The suppression of this pathway inhibited AML cells' proliferation by causing G1 arrest and enhanced AML cells' sensitivity to cytarabine and idarubicin. Similarity, downregulation of CUEDC2 produced opposite results. Knockout or low expression of CUEDC2 in mouse or AML patients displayed lower overall survival and event-free survival rates, compared with these mouse and AML patients had high-CUEDC2 expression. Mechanistic studies revealed that CUEDC2 overexpression attenuated SOCS1 ubiquitination, facilitated its stabilisation by enhancing SOCS1, Elongin C and Cullin-2 (CUL2) interactions, thus inhibited JAK1-STAT3 pathway and leukaemogenesis of AML. Therefore, our novel findings indicated that CUEDC2 interacted with SOCS1 to suppress SOCS1's ubiquitin-mediated degradation, JAK1-STAT3 pathway activation and leukaemogenesis of AML.
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