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Article

Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia

  • Authors:
    • Xiao‑Hui Zhang
    • Lin Yang
    • Xiao‑Jun Liu
    • Ying Zhan
    • Yu‑Xia Pan
    • Xing‑Zhe Wang
    • Jian‑Min Luo
  • View Affiliations / Copyright

    Affiliations: Department of Hematology, The Second Hospital of Hebei Medical University, Key Laboratory of Hematology, Shijiazhuang, Hebei 050000, P.R. China
  • Pages: 1008-1016
    |
    Published online on: June 19, 2018
       https://doi.org/10.3892/or.2018.6508
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Abstract

Suppressor of cytokine signaling‑1 (SOCS1) is a widely recognized tumor suppressor gene. Silencing of SOCS1 expression as a result of promoter methylation is associated with occurrence and development of solid tumors such as liver, cervical and pancreatic cancer. However, the association between SOCS1 gene methylation and acute myeloid leukemia (AML) has not been well explored. In the present study, we examined whether gene expression and methylation status of SOCS1 was altered in AML, and whether this was related to disease occurrence and development. To assess this hypothesis, we analyzed SOCS1 in four groups of AML patients: i) Initial treatment group (IT); ii) relapsed/refractory group (RR); iii) remission group (RE); and iv) normal control group (NC). We also used leukemia cell lines U937 and THP‑1 to study the underlying molecular mechanism of SOCS1 in AML, mainly the JAK2/STAT pathway. We used several techniques such as quantitative PCR (qPCR), methylation‑specific PCR (MS‑PCR), western blotting, flow cytometry and cell transfection techniques to analyze the expression and methylation status of SOCS1. We found that the SOCS1 gene methylation rate in the IT and RR groups was significantly higher than that in the RR and NC groups (48, 80 vs. 0 and 0%, respectively). Furthermore, mRNA and protein expression was significantly lower in the IT and RR groups when compared to the RE and NC groups. We also found that the JAK2/STAT signaling pathway was negatively affected by SOCS1. SOCS1 gene methylation caused gene silencing of SOCS1 which overcame the suppression of the downstream JAK2/STAT signaling pathway by SOCS1, and promoted the growth and proliferation of AML cells.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang XH, Yang L, Liu XJ, Zhan Y, Pan YX, Wang XZ and Luo JM: Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia. Oncol Rep 40: 1008-1016, 2018.
APA
Zhang, X., Yang, L., Liu, X., Zhan, Y., Pan, Y., Wang, X., & Luo, J. (2018). Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia. Oncology Reports, 40, 1008-1016. https://doi.org/10.3892/or.2018.6508
MLA
Zhang, X., Yang, L., Liu, X., Zhan, Y., Pan, Y., Wang, X., Luo, J."Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia". Oncology Reports 40.2 (2018): 1008-1016.
Chicago
Zhang, X., Yang, L., Liu, X., Zhan, Y., Pan, Y., Wang, X., Luo, J."Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia". Oncology Reports 40, no. 2 (2018): 1008-1016. https://doi.org/10.3892/or.2018.6508
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang XH, Yang L, Liu XJ, Zhan Y, Pan YX, Wang XZ and Luo JM: Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia. Oncol Rep 40: 1008-1016, 2018.
APA
Zhang, X., Yang, L., Liu, X., Zhan, Y., Pan, Y., Wang, X., & Luo, J. (2018). Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia. Oncology Reports, 40, 1008-1016. https://doi.org/10.3892/or.2018.6508
MLA
Zhang, X., Yang, L., Liu, X., Zhan, Y., Pan, Y., Wang, X., Luo, J."Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia". Oncology Reports 40.2 (2018): 1008-1016.
Chicago
Zhang, X., Yang, L., Liu, X., Zhan, Y., Pan, Y., Wang, X., Luo, J."Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia". Oncology Reports 40, no. 2 (2018): 1008-1016. https://doi.org/10.3892/or.2018.6508
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