decitabine-induced changes in human myelodysplastic syndrome cell line skm-1 are mediated by foxo3a activation
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ID: 173662
2017
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Abstract
The epigenetic silencing of tumor suppressor genes in myelodysplastic syndromes (MDS) can potentially confer a growth advantage to individual cellular clones. Currently, the recommended treatment for patients with high-risk MDS is the methylation agent decitabine (DAC), a drug that can induce the reexpression of silenced tumor suppressor genes. We investigated the effects of DAC treatment on the myeloid MDS cell line SKM-1 and investigated the role of FOXO3A, a potentially tumor-suppressive transcription factor, by silencing its expression prior to DAC treatment. We found that FOXO3A exists in an inactive, hyperphosphorylated form in SKM-1 cells, but that DAC both induces FOXO3A expression and reactivates the protein by reducing its phosphorylation level. Furthermore, we show that this FOXO3A activation is responsible for the DAC-induced differentiation of SKM-1 cells into monocytes, as well as for SKM-1 cell cycle arrest, apoptosis, and autophagy. Collectively, these results suggest that FOXO3A reactivation may contribute to the therapeutic effects of DAC in MDS.
| Reference Key |
zeng2017journaldecitabine-induced
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|---|---|
| Authors | ;Wen Zeng;Hanjun Dai;Ming Yan;Xiaojun Cai;Hong Luo;Min Ke;Zeming Liu |
| Journal | journal of photochemistry and photobiology b, biology |
| Year | 2017 |
| DOI |
10.1155/2017/4302320
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| URL | |
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