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N6-methyladenosine is the most common modification of eukaryotic RNA. N6-methyladenosine participates in RNA splicing, nuclear export, translation, and degradation through regulation by methyltransferases, methylation readers, and demethylases, affecting messenger RNA stability and translation efficiency. Through the dynamic and reversible regulatory network composed of "writers, erasers, and readers," N6-methyladenosine modification plays a unique role in the process of hematopoiesis. Acute myeloid leukemia is a heterogeneous disease characterized by malignant proliferation of hematopoietic stem cells/progenitor cells. Many studies have shown that N6-methyladenosine–related proteins are abnormally expressed in acute myeloid leukemia and play an important role in the occurrence and development of acute myeloid leukemia, acting as carcinogenic or anticancer factors. Here, we describe the mechanisms of action of reversing N6-methyladenosine modification in hematopoiesis and acute myeloid leukemia occurrence and progression to provide a basis for further research on the role of N6-methyladenosine methylation and its regulatory factors in normal hematopoiesis and acute myeloid leukemia, to ultimately estimate its potential clinical value. [ABSTRACT FROM AUTHOR]

Erratum.

Objective: To explore the mechanism of matrine (Mat) induced human erythroleukemia TF-1 cell apoptosis and its effect on SALL4 expression., Method: Different concentrations of the Mat (0.5, 1.0, 1.5, 2.0 g x L(-1) ) were cultured in vitro in TF-1 cells at different time (24, 48, 72 h). Cell proliferation was assayed by MTT. Cell cycle was determined by flow cytometry (FCM). Cell apoptosis was detected by Annexin V and PI double staining method. SALL4 mRNA expression was detected by reverse transcription RT-PCR (RTT-PCR)., Result: Administrated with Mat (0.5-2.0 g x L(-1)) after 24, 48, 72 h, the proliferation of TF-1 cells were inhibited (P < 0.01) , and in dose- and time-dependent manner. Half inhibitory concentration (IC50 ) was 1.0 g L(-1) at 48 h. After 48 h that the Mat acted on TF-1 cells, the proportion of G0/G1 phase cells increased while compared with the control group, and S phase cells decreased (P < 0.01). Apoptosis were 8.6% , 11.21%, 15.26% , 17.63%, which showed statistically significant difference (P < 0.01) compared with the control group (5.05%). RT-PCR results showed the ratio between SALL4 mRNA expression and beta-actin (internal reference) expression significantly decreased (P < 0.01) with Mat dose increased., Conclusion: In a certain range of concentration and time, Mat can inhibit TFT-1 cells proliferation. The mechanism is to make the cells G0/G1 phase blocked, to inhibit SALL4 gene expression and induce cell apoptosis.