Research
Retinoic acid induces HL-60 cell differentiation via the upregulation of miR-663
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* Corresponding author: Ni Jian Ni_jian2008@163.com
1 Department of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China
2 Hillman Cancer Center Lab, Department of Pathology, Pittsburgh University, G21 5117 Centre Ave. Pittsburgh, PA 15206 USA
3 Translational Research Center, Second Hospital, The Second Clinical School, Nanjing Medical University, Nanjing, China
Journal of Hematology & Oncology 2011, 4:20 doi:10.1186/1756-8722-4-20
Published: 25 April 2011Abstract
Background
Differentiation of the acute myeloid leukemia (AML) cell line HL-60 can be induced by all trans-retinoic acid (ATRA); however, the mechanism regulating this process has not been fully characterized.
Methods
Using bioinformatics and in vitro experiments, we identified the microRNA gene expression profile of HL-60 cells during ATRA induced granulocytic differentiation.
Results
Six microRNAs were upregulated by ATRA treatment, miR-663, miR-494, miR-145, miR-22, miR-363* and miR-223; and three microRNAs were downregulated, miR-10a, miR-181 and miR-612. Additionally, miR-663 expression was regulated by ATRA. We used a lentivirus (LV) backbone incorporating the spleen focus forming virus (SFFV-F) promoter to drive miR-663 expression, as the CMV (Cytomegalovirus) promoter is ineffective in some lymphocyte cells. Transfection of LV-miR-663 induced significant HL-60 cell differentiation in vitro.
Conclusions
Our results show miR-663 may play an important role in ATRA induced HL-60 cell differentiation. Lentivirus delivery of miR-663 could potentially be used directly as an anticancer treatment in hematological malignancies