Abstract
BackgroundBmi-1, the B cell-specific moloney murine leukemia virus insertion site 1, is a member of the Polycomb-group (PcG) family and acts as an oncogene in various tumors; however, its expression related to the prognosis of pediatric patients with acute lymphoblastic leukemia (ALL) has not been well studied.MethodsThe Bmi-1 expression levels in the bone marrow of 104 pediatric ALL patients and 18 normal control subjects were determined by using qRT-PCR. The association between the Bmi-1 expression and the clinicopathological characteristics of pediatric ALL patients was analyzed, and the correlation between Bmi-1 and the prognosis of pediatric ALL was calculated according to the Kaplan–Meier method. Furthermore, the association between Bmi-1 expression and its transcriptional regulator Sall4 was investigated.ResultsCompared to normal control subjects, patients with primary pediatric ALL exhibited upregulated levels of Bmi-1. However, these levels were sharply decreased in patients who achieved complete remission. A significant positive association between elevated Bmi-1 levels and a poor response to prednisone as well as an increased clinical risk was observed. Patients who overexpressed Bmi-1 at the time of diagnosis had a lower relapse-free survival (RFS) rate (75.8%), whereas patients with lower Bmi-1 expression had an RFS of 94.1%. Furthermore, in ALL patients, the mRNA expression of Bmi-1 was positively correlated to the mRNA expression of Sall4a.ConclusionsTaken together, these data suggest that Bmi-1 could serve as a novel prognostic biomarker in pediatric primary ALL and may be partially regulated by Sall4a. Our study also showed that Bmi-1 could serve as a new therapeutic target for the treatment of pediatric ALL.
Highlights
Bmi-1, the B cell-specific moloney murine leukemia virus insertion site 1, is a member of the Polycomb-group (PcG) family and acts as an oncogene in various tumors; its expression related to the prognosis of pediatric patients with acute lymphoblastic leukemia (ALL) has not been well studied
Taken together, these data suggest that Bmi-1 could serve as a novel prognostic biomarker in pediatric primary ALL and may be partially regulated by Sall4a
Our study showed that Bmi-1 could serve as a new therapeutic target for the treatment of pediatric ALL
Summary
Bmi-1, the B cell-specific moloney murine leukemia virus insertion site 1, is a member of the Polycomb-group (PcG) family and acts as an oncogene in various tumors; its expression related to the prognosis of pediatric patients with acute lymphoblastic leukemia (ALL) has not been well studied. Acute lymphoblastic leukemia (ALL) is a common pediatric malignant tumor characterized by the overproduction and accumulation of immature lymphoid cells and accounts for nearly 25% of all cancers among children younger than 15 years old [1]. The Bmi-1 (B cell-specific moloney murine leukemia virus integration site 1) gene is a recognized oncogene of the Polycomb-group (PcG) family and was originally identified via retroviral insertional mutagenesis in Eμ-cmyc transgenic mice that were infected with the Moloney murine leukemia virus [4, 5]. Bmi-1 has been implicated to play a critical role in a number of biological pathways, including stem cell self-renewal
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