Abstract
To uncover the biological role of lncRNA DCST1-AS1 in the process of pediatric AML and its regulatory effect on p53 methylation. Serum level of DCST1-AS1 in AML children and healthy participants was detected by qRT-PCR. The role of DCST1-AS1 in mediating biological functions of AML193 and U937 cells was assessed by functional experiments. p53 methylation level was examined. Through BSP, MSP and dual-luciferase reporter assay, the regulatory effect of DCST1-AS1 on p53 methylation was explored. The correlation between DCST1-AS1 and p53 in the serum of AML children was assessed. Serum level of DCST1-AS1 was higher in AML children than in healthy subjects. Knockdown of DCST1-AS1 decreased proliferative and migratory rates in AML193 and U937 cells. DCST1-AS1 was able to induce methylation of p53 promoter. P53 was markedly upregulated by the knockdown of DCST1-AS1, presenting a negative correlation. LncRNA DCST1-AS1 drives the malignant progression of pediatric AML through inducing methylation of the p53 promoter.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
