Regular ArticleMonocytically Differentiating HL60 Cells Proliferate Rapidly before They Mature
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2016, Cell ReportsCitation Excerpt :These findings led to in vivo studies and phase 1 clinical trials for the use of vitamin D as a differentiation agent for acute myeloid leukemia (AML), which ultimately proved to be unsuccessful because of hypercalcemia and heterogeneity of the AML subtypes tested (Marchwicka et al., 2014). Interestingly, although treatment of the HL-60 leukemia cell line with 1,25(OH)D3 required 18–20 hr of exposure for differentiation to begin (Mangelsdorf et al., 1984), an initial burst in proliferation was seen during early phases (Brown et al., 1999), similar to the effect on HSPCs observed here. Our data indicate that 1,25(OH)D3 stimulates proliferative HSPC expansion.
Natural compounds and pharmaceuticals reprogram leukemia cell differentiation pathways
2015, Biotechnology AdvancesCitation Excerpt :Moreover, transcription factors, including CCAAT/enhancer binding protein (C/EBP)α, RUNX1 and E proteins (Gentleman et al., 2004; Koschmieder et al., 2009; Tang et al., 2009; Wouters et al., 2009), and the epigenetic regulatory proteins HDACs, CBP/p300, PRMT1 and SON are reportedly involved in the initiation/progression of t(8;21) AML–M2 (Gelmetti et al., 1998; Shia et al., 2012). The anti-cancer activities of the active form of vitamin D, 1,25-dihydroxyvitamin D3 (VD3) (1), have long been linked to the ability of this compound to induce the differentiation of human myeloid leukemia cells into monocyte–macrophages (Brown et al., 1999; Okamoto et al., 2008), including in pro-myelocytic HL60, mouse myeloblastic leukemia M1 and histiocytic monoblast-like lymphoma U937 cells (Abe et al., 1981; Tanaka et al., 1983). VD3 (1) activates several signaling pathways, such as the MAPK and PI3K/AKT pathways, as well as lipid signaling pathways (Marchwicka et al., 2014).
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2012, Cancer LettersCitation Excerpt :Thus, the anti-proliferative and terminally-differentiating effects of vitamin D and analogs have become a focal point of investigation for the treatment of hematological malignancies, especially AML. The complexity of the initiation of vitamin D-induced differentiation and its relation to cell cycle systems was indicated in the observation that HL-60 cells initially responded to 1,25D treatment by proliferating rapidly prior to eventual growth arrest and monocytic differentiation [7]. This early proliferative burst was also observed in U937 cells, followed by elevated levels of specific cyclin-dependent kinase inhibitors, p21Waf1/Cip1 and p27Kip1.
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