ORIGINAL RESEARCH PAPER Complementary analysis of microRNA and mRNA expression during phorbol 12-myristate 13-acetate (TPA)-induced differentiation of HL-60 cells Ailiang Chen Æ Mingyong Luo Æ Guohua Yuan Æ Jian Yu Æ Tuo Deng Æ Liang Zhang Æ Yuxiang Zhou Æ Keith Mitchelson Æ Jing Cheng Received: 15 May 2008 / Revised: 23 June 2008 / Accepted: 24 June 2008 / Published online: 22 July 2008 Ó Springer Science+Business Media B.V. 2008 Abstract MicroRNAs (miRNAs) and mRNAs con- stitute an important part of gene regulatory networks, influencing diverse biological phenomena. To dis- cover novel regulatory pathways during myeloid differentiation, we performed miRNA as well as mRNA expression profiling of in vitro-differentiating HL-60 cells treated with 12-O-tetradecanoylphorbol- 13-acetate (TPA). The main findings were up-regula- tion of miR-146a/b, miR-21, miR-221, miR-222, miR-155, miR-26a and down-regulation of miR- 199a*, miR-181c, miR-142-3p, miR-92. After integrat- ing the miRNA and mRNA expression data into a Transcriptome Interaction Database by Molecule Anno- tation System (MAS) software, a number of differently expressed mRNAs were revealed as potential targets of these miRNAs. Keywords Cell differentiation Á HL-60 Á Microarray Á MicroRNA Á TPA Introduction Acute promyelocytic leukemia (APL) is characterized by a neoplastic proliferation of myeloid cells. The malignant cells have a differentiation block at the promyelocyte stage which results in an accumulation of immature cells (Bruserud and Gjertsen 2000). The human promyelocytic leukemia cell line HL-60, derived from a patient with acute promyelocytic leukemia, can be induced in vitro to differentiate towards a variety of different cell types of the myelomonocytic lineage (Collins 1987). The tumor promoter, phorbol 12-myristate 13-acetate (TPA) is an extraordinarily potent stimulator of differentiation of HL-60 cells in vitro (Goel et al. 2007). TPA can inhibit Electronic supplementary material The online version of this article (doi:10.1007/s10529-008-9800-8) contains supplementary material, which is available to authorized users. A. Chen Á J. Yu Á T. Deng Á Y. Zhou Á K. Mitchelson (&) Á J. Cheng (&) Medical Systems Biology Research Center, Tsinghua University School of Medicine, Beijing 100084, Peoples’ Republic of China e-mail: kmitchelson@tsinghua.edu.cn J. Cheng e-mail: jcheng@tsinghua.edu.cn A. Chen Á J. Yu Á T. Deng Á Y. Zhou Á J. Cheng Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, Peoples’ Republic of China A. Chen Á M. Luo Á J. Yu Á T. Deng Á L. Zhang Á Y. Zhou Á K. Mitchelson Á J. Cheng National Engineering Research Center for Beijing Biochip Technology & CapitalBio Corporation, 18 Life Science Parkway, Changping District, Beijing 102206, Peoples’ Republic of China G. Yuan Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, Peoples’ Republic of China 123 Biotechnol Lett (2008) 30:2045–2052 DOI 10.1007/s10529-008-9800-8