KMOE-2
Cat.No.: CSC-C0213
Species: Homo sapiens (Human)
Source: Blood; Peripheral Blood
Morphology: single, large, round to oval cells in suspension
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KMOE-2 is a continuous human erythroid leukaemia cell line established in 1978 from peripheral blood of a 2-year-old female patient with acute erythremia (Di Guglielmo's illness). It has a hypotetraploid karyotype (modal number 82, range 80-88) and develops in suspension as solitary, big, round to oval cells.
KMOE-2 cells are cultured in conventional conditions (37°C, 5% CO2) in a nutrient-rich basal medium supplemented with serum. Their doubling time is about 40-50 h. They are seeded at a density of 0.2-0.4 × 10 6 cells/mL and achieve a peak density of about 0.6 × 10 6 cells/mL.
One of the characteristics of KMOE-2 is its erythroid differentiation potential. When treated with metabolic inhibitors such as cytosine arabinoside, the cells could synthesize hemoglobin and show benzidine-positive phenotypes. Therefore, this cell line is a useful model for researching erythropoiesis, processes of leukemic cell differentiation and screening of new therapeutic drugs against hematologic malignancies.
NFE2 Is Regulated via JAK2-Mediated Histone Tyrosine Phosphorylation
NFE2 is frequently overexpressed in myeloproliferative neoplasms (MPNs) and drives disease progression in murine models, yet its upstream regulators and downstream effectors remain unclear. Peeken et al. investigated how epigenetic modifications, specifically histone methylation and phosphorylation, regulate NFE2 expression.
They examined the role of JAK2-mediated phosphorylation. JAK2 phosphorylates Histone H3 at Tyrosine 41 (H3Y41), disrupting Heterochromatin Protein 1α (HP1α) binding. The NFE2-1A promoter harbored phospho-H3Y41, and this mark was significantly reduced by decitabine treatment.
To assess the role of JAK2 mutational status, they compared JAK2V617F mutant cell lines (HEL, UKE-1, SET-2) with JAK2 wild-type (wt) lines (K562, KMOE-2). Decitabine effectively silenced NFE2 and reduced H3K9me2 at its promoters in JAK2V617F mutant cells (Fig. 1A-C). In contrast, decitabine had no significant effect on NFE2 levels or H3K9me2 marks in JAK2wt cells (Fig. 1A, B, D). These findings indicate that decitabine selectively targets NFE2 expression in cells harboring the JAK2V617F mutation.
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