Identification of the C/EBPα C-terminal tail residues involved in the protein interaction with GABP and their potency in myeloid differentiation of K562 cells

Shimokawa, Toshibumi; Nunomura, Satoshi; Fujisawa, Daisuke; Ra, Chisei

doi:10.1016/j.bbagrm.2013.09.004

Cited by 8 publications

(6 citation statements)

References 44 publications

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“…This analysis predicted positive connectivity between the C/EBPα activation signature and histone deacetylase inhibitors. The results showed that histone deacetylase inhibitors reactivated the expression of the C/EBPα signature and promoted granulocytic differentiation of primary samples from the C/EBPα dysfunctional subset harboring biallelic C/EBPα mutations (66), which indicated that HDAC inhibitors could represent a promising therapeutic approach in this particular subtype of AML (67,68). Cytarabine (or Ara-C) is a pyrimidine antagonist, which interferes with DNA synthesis and is used in upfront and salvage regimens for AML (69).…”

Section: Regulators Targeting C/ebpα In Myeloid Differentiation and Lmentioning

confidence: 99%

Regulation of the C/EBPα signaling pathway in acute myeloid leukemia (Review)

Song

Wang

et al. 2015

Oncology Reports

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The transcription factor CCAAT/enhancer binding protein α (C/EBPα), as a critical regulator of myeloid development, directs granulocyte and monocyte differentiation. Various mechanisms have been identified to explain how C/EBPα functions in patients with acute myeloid leukemia (AML). C/EBPα expression is suppressed as a result of common leukemia-associated genetic and epigenetic alterations such as AML1-ETO, RARα-PLZF or gene promoter methylation. Recent data have shown that ubiquitination modification also contributes to its downregulation. In addition, 10-15% of patients with AML in an intermediate cytogenetic risk subgroup were characterized by mutations of the C/EBPα gene. As a transcription factor, C/EBPα can translocate into the nucleus and further regulate a variety of genes directly or indirectly, which are all key factors for cell differentiation. This review summarizes recent reports concerning the dysregulation of C/EBPα expression at various levels in human AML. The currently available data are persuasive evidence suggesting that impaired abnormal C/EBPα expression contributes to the development of AML, and restoration of C/EBPα expression as well as its function represents a promising target for novel therapeutic strategies in AML.

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Section: Regulators Targeting C/ebpα In Myeloid Differentiation and Lmentioning

confidence: 99%

Regulation of the C/EBPα signaling pathway in acute myeloid leukemia (Review)

Song

Wang

et al. 2015

Oncology Reports

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“…Recently, it was reported that CEBP‐ẟ regulated VEGF‐C (a member of the VEGF family) autocrine signaling . On the other hand, GABP was found to interact with CEBP in the regulation of K562 cell differentiation . Additionally, GABP regulated the expression of VEGF in a mouse ocular neovascularization model.…”

Section: Discussionmentioning

confidence: 99%

“…26 On the other hand, GABP was found to interact with CEBP in the regulation of K562 cell differentiation. 27 Additionally, GABP regulated the expression of VEGF in a mouse ocular neovascularization model. Transfection of the human GABP gene into conjunctival epithelial cells resulted in reduced VEGF expression.…”

Section: Discussionmentioning

confidence: 99%

The VEGFA ‐1154G/A polymorphism is associated with reduced risk of rheumatoid arthritis but not with systemic lupus erythematosus in Mexican women

Ramírez‐Bello

Cadena-Sandoval

Fragoso

et al. 2018

The Journal of Gene Medicine

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“…C/EBPα plays an important role in the proliferation and differentiation of granulocytes [18,19,20]. In C/EBPα knockout mice, myeloid cell differentiation is completely stagnated in the progenitor cell stage, suggesting that C/EBPα is involved in the formation of myeloid cells [21].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of CCAAT Enhancer-Binding Protein α Inhibits the Growth of K562 Cells via the Foxo3a-Bim Pathway

Zhang

Dong²,

Luan³

et al. 2016

Acta Haematol

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We aimed to investigate the role of CCAAT enhancer-binding protein α (C/EBPα) in the pathogenesis of chronic myeloid leukemia (CML) and the mechanism underlying its effect. Bone marrow specimens from 50 patients with CML and peripheral blood specimens from 20 healthy individuals were collected. K562 cells were treated with imatinib. Subsequently, a stable cell line, K562-C/EBPα, was constructed. Cell proliferation was assayed with cell counting kit-8, and mRNA levels of C/EBPα, forkhead transcription factor FKHRL1 (Foxo3a) and Bim were detected by semiquantitative PCR. The correlation of C/EBPα and BCR-ABL was assessed by Spearman's correlation analysis. The results showed that C/EBPα mRNA levels were significantly reduced in CML patients compared with healthy subjects (p < 0.001) and were negatively correlated with BCR-ABL1 (r = -0.5046, p < 0.01). Additionally, imatinib enhanced the expression of C/EBPα in K562 cells compared with untreated cells (p < 0.05). Overexpression of C/EBPα significantly decreased cell proliferation and upregulated the expressions of the apoptosis-related genes Foxo3a (p < 0.01) and Bim (p < 0.05) in K562 cells. In conclusion, C/EBPα expression was decreased in patients with CML. Imatinib enhances the expression of C/EBPα in K562 cells, and the overexpression of C/EBPα inhibits cell proliferation and increases apoptosis via the Foxo3a-Bim pathway.

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Identification of the C/EBPα C-terminal tail residues involved in the protein interaction with GABP and their potency in myeloid differentiation of K562 cells

Cited by 8 publications

References 44 publications

Regulation of the C/EBPα signaling pathway in acute myeloid leukemia (Review)

Regulation of the C/EBPα signaling pathway in acute myeloid leukemia (Review)

The VEGFA ‐1154G/A polymorphism is associated with reduced risk of rheumatoid arthritis but not with systemic lupus erythematosus in Mexican women

Overexpression of CCAAT Enhancer-Binding Protein α Inhibits the Growth of K562 Cells via the Foxo3a-Bim Pathway

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