Dynamic transcriptomes of human myeloid leukemia cells

Hai Wang, Haiyan Hu, Qian Zhang, Yadong Yang, Yanming Li, Yang Hu, Xiuyan Ruan, Yaran Yang, Zhaojun Zhang, Chang Shu, Jiangwei Yan, Edward K. Wakeland, Quanzhen Li, Songnian Hu, Xiangdong Fang

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

To identify the mechanisms controlling chronic myeloid leukemia (CML) and acute myeloid leukemia (AML) in humans, we analyzed genome-wide transcription dynamics in three myeloid leukemia cell lines (K562, HL-60, and THP1) using high-throughput sequencing technology. Using KEGG analysis, we found that the ERK/MAPK, JAK-STAT and ErbB pathways promoted proliferation and metabolism in CML. However, in AML, differentiation and apoptosis blocking resulted in the accumulation of blast cells in marrow. In addition, each cell type had unique characteristics. K562 cells are an ideal model for studying erythroid differentiation and globin gene expression. The chemokine signaling pathway and Fc gamma R-mediated phagocytosis were markedly upregulated in HL-60 cells. In THP1 cells, highly expressed genes ensured strong phagocytosis by monocytes. Further, we provide a new insight into myeloid development. The abundant data sets and well-defined analysis methods will provide a resource and strategy for further investigation of myeloid leukemia. •We identified the different pathways between CML and AML.•Different myeloid cells have unique functional characteristics.•Distinct gene expression patterns are found during myeloid development.

Original languageEnglish (US)
Pages (from-to)250-256
Number of pages7
JournalGenomics
Volume102
Issue number4
DOIs
StatePublished - Oct 1 2013

Keywords

  • Acute myeloid leukemia
  • Chronic myeloid leukemia
  • High-throughput RNA sequencing

ASJC Scopus subject areas

  • Genetics

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    Wang, H., Hu, H., Zhang, Q., Yang, Y., Li, Y., Hu, Y., Ruan, X., Yang, Y., Zhang, Z., Shu, C., Yan, J., Wakeland, E. K., Li, Q., Hu, S., & Fang, X. (2013). Dynamic transcriptomes of human myeloid leukemia cells. Genomics, 102(4), 250-256. https://doi.org/10.1016/j.ygeno.2013.06.004