Abstract

Leukocyte differentiation antigens often represent important markers for the diagnosis, classification, prognosis, and therapeutic targeting of myeloid leukemia. Herein, we report a potential leukocyte differentiation antigen gene VSTM1 (V-set and transmembrane domain-containing 1) that was downregulated in bone marrow cells from leukemia patients and exhibited a higher degree of promoter methylation. The expression level of its predominant encoded product, VSTM1-v1, was positively correlated with myeloid cell maturation state. Restoration of VSTM1-v1 expression inhibited myeloid leukemia cells’ growth. Therefore, VSTM1-v1 might represent an important myeloid leukocyte differentiation antigen and provide a potential target for the diagnosis and treatment of leukemia.Electronic supplementary materialThe online version of this article (doi:10.1186/s13045-015-0118-4) contains supplementary material, which is available to authorized users.

Highlights

  • Leukocyte differentiation antigens often represent important markers for the diagnosis, classification, prognosis, and therapeutic targeting of myeloid leukemia

  • VSTM1 (V-set and transmembrane domain-containing 1) encodes a potential leukocyte differentiation antigen that is highly expressed in myeloid cells, but silenced in multiple leukemia cell lines [1]

  • To determine whether it plays a role in leukemogenesis, we characterized its expression pattern and function in bone marrow cells from Acute myeloid leukemia (AML)/chronic myeloid leukemia (CML) patients and myeloid leukemia cell lines

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Summary

Untreated CML

MIC morphological, immunological, and cytogenetic classifications, n.a. not available due to a small sample size. aThe P value was calculated using Wilcoxon signed ranks test as compared to the HD group. Using CD16 and CD14 as phenotypic markers for mature granulocytes and monocytes, respectively, we found a similar result (Additional file 1: Table S2). This correlation was subsequently confirmed by increased VSTM1 expression in bone marrow cells from APL patients and in NB4 cells after ATRA treatment in vitro (Additional file 5: Figure S4). These findings provide a potential reason why VSTM1 expression levels were reduced so markedly in AML and CML-AP/BC patients. When searching for clinical features that could be related to VSTM1 expression in AML patients, we detected a higher expression level of

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