Induction of Differentiation in K562 Cell Line by Nicotinic Acid-Related Compounds

Ida, Chieri; Ogata, Shin; Okumura, Katsuhiko; Taguchi, Hiroshi

doi:10.1271/bbb.80483

Cited by 9 publications

(13 citation statements)

References 22 publications

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“…As previously reported NAD-precursors such as NA and other niacin-related compounds induce differentiation in immortalized cell lines, such as K562 and HL60 (Ida et al, 2009, Iwata et al, 2003. These findings prompted us to assess morphological changes upon NAD treatment.…”

Section: Nad Induces Myeloid Differentiationmentioning

confidence: 80%

“…NAD precursors drive myeloid differentiation and impair cell growth (Ida et al, 2009, Iwata et al, 2003. To examine whether similar effects could be mediated by NAD, K562 cells were cultured following a single addition of NAD or vehicle to the media, and tracked over four days (Fig.…”

Section: Nad Inhibits Cancer Cell Growth In a Dose-dependent Manner Amentioning

confidence: 99%

“…Maintenance of adequate levels of NAD is critical for cellular function and genomic stability (Ralto, Rhee et al, 2020). Few reports have shown that NAD precursors such as vitamin B3 (or nicotinic acid, NA) and nicotinamide (Nam) are able to drive cell differentiation in leukemic cell lines (Ida, Ogata et al, 2009, Iwata, Ogata et al, 2003, and impair cell growth. However, the molecular mechanism participating in these morphological changes remain unknown.…”

Section: Introductionmentioning

confidence: 99%

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NAD modulates DNA methylation and cell differentiation

Ummarino

Bassal

Zhang

et al. 2020

Preprint

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Nutritional intake impacts the human epigenome by directing epigenetic pathways in normal cell development via as yet unknown molecular mechanisms. Consequently, imbalance in the nutritional intake is able to dysregulate the epigenetic profile and drive cells towards malignant transformation. Herein, we present a novel epigenetic effect of the essential nutrient, NAD. We demonstrate that impairment of DNMT1 enzymatic activity by NAD-promoted ADP-ribosylation, leads to demethylation and transcriptional activation of CEBPA gene, suggesting the existence of an unknown NAD-controlled region within the locus. In addition to the molecular events, NAD treated cells exhibit significant morphological and phenotypical changes that correspond to myeloid differentiation.Collectively, these results delineate a novel role for NAD in cell differentiation and indicate novel nutri-epigenetic strategy to regulate and control gene expression in human cells.

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Section: Nad Induces Myeloid Differentiationmentioning

confidence: 80%

Section: Nad Inhibits Cancer Cell Growth In a Dose-dependent Manner Amentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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NAD modulates DNA methylation and cell differentiation

Ummarino

Bassal

Zhang

et al. 2020

Preprint

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“…K562 cells are human immortalized myelogenous leukemia cells obtained from the pleural fluid of patients with chronic myeloid leukemia in blast crisis [ 17 ]. These cells have been useful for studying hematopoietic cell proliferation and differentiation [ 18 ] and can differentiate into an erythroid lineage when treated with differentiation-inducing reagents such as hemin, sodium butyrate, and nicotinic acid [ 19 , 20 ]. The induced cells produce hemoglobin, and differentiation can be validated by benzidine staining or hemoglobin quantification [ 18 , 21 – 23 ].…”

Section: Introductionmentioning

confidence: 99%

Voltage-Gated K+ Channel, Kv3.3 Is Involved in Hemin-Induced K562 Differentiation

et al. 2016

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Voltage-gated K+ (Kv) channels are well known to be involved in cell proliferation. However, even though cell proliferation is closely related to cell differentiation, the relationship between Kv channels and cell differentiation remains poorly investigated. This study demonstrates that Kv3.3 is involved in K562 cell erythroid differentiation. Down-regulation of Kv3.3 using siRNA-Kv3.3 increased hemin-induced K562 erythroid differentiation through decreased activation of signal molecules such as p38, cAMP response element-binding protein, and c-fos. Down-regulation of Kv3.3 also enhanced cell adhesion by increasing integrin β3 and this effect was amplified when the cells were cultured with fibronectin. The Kv channels, or at least Kv3.3, appear to be associated with cell differentiation; therefore, understanding the mechanisms of Kv channel regulation of cell differentiation would provide important information regarding vital cellular processes.

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“…7,8) We have found that two nicotinic acid-related compounds, nicotinic acid and isonicotinic acid, induced erythroid differentiation in K562 cells. 9) To elucidate the mechanism for erythroid differentiation in K562 cells, we focused on the alteration of intracellular NAD content during differentiation. In this study, we investigated changes in the NAD content induced by nicotinic acidrelated compounds in K562 cells undergoing differentiation.…”

mentioning

confidence: 99%

Changes in NAD Content Induced by Nicotinic Acid-Related Compounds in K562 Cells during Differentiation

Ida

Ogata

2013

Bioscience, Biotechnology, and Biochemistry

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Two nicotinic acid-related compounds were found to induce erythroid differentiation in K562 cells. We investigated the changes in nicotinamide adenine dinucleotide (NAD) content induced by nicotinic acid-related compounds during differentiation. The NAD content was reduced by a treatment with nicotinic acid and isonicotinic acid. These results provide important clues toward elucidating the erythroid differentiation mechanism.

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Induction of Differentiation in K562 Cell Line by Nicotinic Acid-Related Compounds

Cited by 9 publications

References 22 publications

NAD modulates DNA methylation and cell differentiation

NAD modulates DNA methylation and cell differentiation

Voltage-Gated K+ Channel, Kv3.3 Is Involved in Hemin-Induced K562 Differentiation

Changes in NAD Content Induced by Nicotinic Acid-Related Compounds in K562 Cells during Differentiation

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