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Retinoic acid induces HL-60 cell differentiation via the upregulation of miR-663

Jian, P and Li, ZW and Fang, TY and Jian, W and Zhuan, Z and Mei, LX and Yan, WS and Jian, N (2011) Retinoic acid induces HL-60 cell differentiation via the upregulation of miR-663. Journal of Hematology and Oncology, 4.

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Abstract

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. © 2011 Jian et al; licensee BioMed Central Ltd.

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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Jian, P
Li, ZW
Fang, TY
Jian, W
Zhuan, Z
Mei, LX
Yan, WS
Jian, N
Centers: Other Centers, Institutes, Offices, or Units > Hillman Cancer Center
Date: 23 May 2011
Date Type: Publication
Journal or Publication Title: Journal of Hematology and Oncology
Volume: 4
DOI or Unique Handle: 10.1186/1756-8722-4-20
Schools and Programs: School of Medicine > Pathology
Refereed: Yes
Date Deposited: 31 Oct 2016 16:06
Last Modified: 29 Jan 2019 15:55
URI: http://d-scholarship.pitt.edu/id/eprint/30072

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