Pathways related to PMA-differentiated THP1 human monocytic leukemia cells revealed by RNA-Seq

Pathways related to PMA-differentiated THP1 human monocytic leukemia cells revealed by RNA-Seq
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RNA-Seq揭示与PMA分化的THP1人单核细胞白血病细胞相关的通路

DOI:
10.1007/s11427-015-4967-4
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发表时间:
2015-12-01
影响因子:
9.1
通讯作者:
Li YangQiu,Yangqiu
Li YangQiu,Yangqiu
中科院分区:
生物学1区
文献类型:
--
作者:
Zeng ChengWu,Chengwu;Wang WenTao,Wentao;Li YangQiu,Yangqiu

文献摘要

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已有研究报道佛波酯(PMA)可将人单核细胞系THP1分化为具有巨噬细胞样特征的细胞。然而,人们对调控这种分化过程的机制知之甚少。在这里,我们进行了高通量RNA-Seq分析,以研究经PMA处理和未经PMA处理的THP1细胞中差异表达的基因,并检测那些可能与PMA诱导单核细胞向巨噬细胞分化有关的基因。我们发现,在PMA治疗后,有3000个基因有差异表达。基因本体论分析表明,与细胞过程和生物过程调控相关的基因显著丰富。KEGG分析还表明,差异表达基因(DEG)在PI3K/AKT信号通路和吞噬小体通路中显著丰富。重要的是,我们揭示了PI3K/AKT通路在PMA诱导的THP1细胞分化中的重要作用。所确定的DEGS和途径可能有助于进一步研究THP1分化的详细分子机制。因此,我们的结果为调节这种疾病的分化提供了许多潜在的治疗靶点。
Previous analyses have reported that the human monocytic cell line THP1 can be differentiated into cells with macrophage-like characteristics by phorbol 12-myristate 13-acetate (PMA). However, little is known about the mechanism responsible for regulating this differentiation process. Here, we performed high-throughput RNA-Seq analysis to investigate the genes differently expressed in THP1 cells treated with and without PMA and examined those that may be responsible for the PMA-induced differentiation of monocytes into macrophages. We found 3,000 genes to be differentially expressed after PMA treatment. Gene ontology analysis revealed that genes related to cellular processes and regulation of biological processes were significantly enriched. KEGG analysis also demonstrated that the differentially expressed genes (DEGs) were significantly enriched in the PI3K/AKT signaling pathway and phagosome pathway. Importantly, we reveal an important role of the PI3K/AKT pathway in PMA-induced THP1 cell differentiation. The identified DEGs and pathways may facilitate further study of the detailed molecular mechanisms of THP1 differentiation. Thus, our results provide numerous potential therapeutic targets for modulation of the differentiation of this disease.