Ara-C elicits apoptosis and inhibits proliferation of human lymphoblastic leukemia Nalm6 cell lines by down regulation of HDAC3 and DNMT3B and up regulation of DNMT3A

Moghadasi, Soudeh; Pourrajab, Fatemeh; Hekmatimoghaddam, Seyedhossein

doi:10.4993/acrt.29.47

Ann. Cancer Res. Therap.

2021

DOI: 10.4993/acrt.29.47

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Ara-C elicits apoptosis and inhibits proliferation of human lymphoblastic leukemia Nalm6 cell lines by down regulation of HDAC3 and DNMT3B and up regulation of DNMT3A

Soudeh Moghadasi

Fatemeh Pourrajab

Seyedhossein Hekmatimoghaddam

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2024

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Azacitidine and cytarabine induce sustained lymphopenia with abnormal differentiation of common lymphoid progenitors and prolonged suppression of Dnmt3a and Dnmt3b expression in mice

Matsushita,

Miwa,

Sato

et al. 2024

Toxicological Sciences

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Myelosuppression is a major side effect of chemotherapy. Although decreased blood cells are restored with the recovery of bone marrow cells, insufficient recovery of decreased lymphocytes was observed in mice given azacitidine (AZA), a DNA methyltransferase (DNMT) inhibitor, even following the restoration of bone marrow cells. To understand the mechanisms behind this sustained lymphopenia, we examined AZA’s impact on the hematopoietic progenitor cells and the expression of Dnmts and differentiation-related genes. An antimetabolite of cytidine analog, cytarabine (Ara-C), was used as a reference compound. Decreases in almost all blood parameters and common lymphoid progenitors (CLPs) and the downregulation of Dnmts and differentiation-related genes in Lineage−Sca-1+c-kit+ (LSK) cells were observed in mice administered AZA or Ara-C for 7 d. In the posttreatment observation, all parameters, except for lymphocytes and monocytes, exhibited recovery within 3 wk after the final dosing in both treated groups. However, no recovery from the decreases in lymphocytes, especially B cells, and monocytes occurred even after 5 wk. The number of CLPs was elevated after 3 wk. There was a tendency toward recovery from the decreased expression of Dnmt1 and differentiation-related genes, but the expression levels of Dnmt3a and Dnmt3b did not fully recover even 5 wk after the final dosing. Taken together, the findings revealed that the mechanism of sustained lymphopenia observed in mice treated with AZA or Ara-C is associated, at least in part, with the abnormal differentiation of CLPs into B cells accompanied by the prolonged suppression of Dnmt3a and Dnmt3b expression on LSK cells.

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Azacitidine and cytarabine induce sustained lymphopenia with abnormal differentiation of common lymphoid progenitors and prolonged suppression of Dnmt3a and Dnmt3b expression in mice

Matsushita,

Miwa,

Sato

et al. 2024

Toxicological Sciences

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show abstract

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Ara-C elicits apoptosis and inhibits proliferation of human lymphoblastic leukemia Nalm6 cell lines by down regulation of HDAC3 and DNMT3B and up regulation of DNMT3A

Cited by 1 publication

References 25 publications

Azacitidine and cytarabine induce sustained lymphopenia with abnormal differentiation of common lymphoid progenitors and prolonged suppression of Dnmt3a and Dnmt3b expression in mice

Azacitidine and cytarabine induce sustained lymphopenia with abnormal differentiation of common lymphoid progenitors and prolonged suppression of Dnmt3a and Dnmt3b expression in mice

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