摘要：The thalassemia of Hemoglobin H-Constant Spring disease (HbH-CS) is the most common type of Thalassemia in non-transfusion thalassemia. Interestingly, the clinical manifestations of the same genotype of thalassemia can be vastly different, likely due to epigenetic regulation. Here, we used microarray technology to reveal the epigenetic regulation of m
6A in modifiable diseases and demonstrated a role of
BCL2A1
in disease regulation. In this study, we revealed that methylating enzyme writers including
METTL16
,
WTAP, CBLL1, RBM15B,
and
ZC3H13
displayed low expression and the demethylating enzyme
ALKBH5
, along with reader proteins including
IGF2BP2
and
YTHDF3
exhibited high expression. In addition,
BCL2A1
was hypo-methylated and showed low expression. We also revealed that the
BCL2A1
methylation level and
IGF2BP2
expression were negatively correlated. Additionally, the mRNAs expression between
ALKBH5
and
IGF2BP2
were positively correlated. In HbH-CS, most genes were hypo-methylated. This included
BCL2A1
, which may play an important role in the process of red blood cell differentiation and development of HbH-CS. Moreover, the mRNA-M
6A methylation status may be regulated by the demethylating enzyme
ALKBH5
via
IGF2BP2
.
