Background and purpose: Suppressor of cytokine signaling 1 (SOCS1) is a widely recognized tumor suppressor gene. This study aimed to explore the relationship between the epigenetic modification of SOCS1 gene and acute myeloid leukemia (AML). Methods: We utilized several techniques such as reverse transcription polymerase chain reaction (RT-PCR)

methylation-specific PCR (MS-PCR)

Western blot

cell culture

drug treatment

cell viability assay and gene knock-out to analyze the expression of SOCS1. We analyzed 110 AML patients treated in the Department of Hematology

Handan Central Hospital

and Department of Hematology

The Second Hospital of Hebei Medical University

from Feb. 2016 to Dec. 2018

and leukemia cell lines U937 and THP-1 to study the underlying molecular mechanism of SOCS1 in AML. We also utilized the changes of DNA methyltransferase 1 (DNMT1)

DNA methyltransferase 3a (DNMT3a) and histone deacetylase 1 (HDAC1). Results: We found that SOCS1 gene methylation rate in initial treatment group (IT) and relapsed/refractory group (RR) group was significantly higher than that in remission group (RE) and normal control group (NC) (48% and 80% vs 0% and 0% respectively). Moreover

the mRNA and protein expression were significantly lower in IT and RR when compare to RE and NC. We also found that the expressions of DNMT1

DNMT3a and HDAC1 were negatively affected by SOCS1. SOCS1 methylation was negatively correlated with complete remission (CR) after treatment. After drug treatment

the growth of tumor cells was inhibited with the decrease of DNMT1

DNMT3a and HDAC1 expressions and the recovery of SOCS1 gene expression. Conclusion: SOCS1 gene methylation and deacetylation caused gene silencing of SOCS1 which promoted the growth and proliferation of acute myeloid leukemia cells.