TY - JOUR
T1 - Dynamic transcriptomes of human myeloid leukemia cells
AU - Wang, Hai
AU - Hu, Haiyan
AU - Zhang, Qian
AU - Yang, Yadong
AU - Li, Yanming
AU - Hu, Yang
AU - Ruan, Xiuyan
AU - Yang, Yaran
AU - Zhang, Zhaojun
AU - Shu, Chang
AU - Yan, Jiangwei
AU - Wakeland, Edward K.
AU - Li, Quanzhen
AU - Hu, Songnian
AU - Fang, Xiangdong
N1 - Funding Information:
This research was supported by the National Key Scientific Instrument and Equipment Development Projects of China ( 2011YQ03013404 to X.F.); the National Basic Research Program (973 Program) ( 2006CB910401 and 2006CB910403 to S.H.); the “Strategic Priority Research Program” of the Chinese Academy of Sciences, Stem Cell and Regenerative Medicine Research ( XDA01040405 to X.F.), the Knowledge Innovation Program of the Chinese Academy of Sciences KSCX2-EW-R-01-04 to S.H.); Chinese Academy of Sciences Visiting Professorship for Senior International Scientists ( 2010T2S20 ) and the High-end Foreign Experts Talents Program ( GDJ20120491014 ) to E.K.W.
PY - 2013/10
Y1 - 2013/10
N2 - 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.
AB - 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.
KW - Acute myeloid leukemia
KW - Chronic myeloid leukemia
KW - High-throughput RNA sequencing
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U2 - 10.1016/j.ygeno.2013.06.004
DO - 10.1016/j.ygeno.2013.06.004
M3 - Article
C2 - 23806289
AN - SCOPUS:84886304334
SN - 0888-7543
VL - 102
SP - 250
EP - 256
JO - Genomics
JF - Genomics
IS - 4
ER -