DDIT4 mediates the proliferation-promotive effect of IL-34 in human monocytic leukemia cells.

IF 1.5 Q3 HEMATOLOGY 血液科学(英文) Pub Date : 2021-04-27 eCollection Date: 2021-04-01 DOI:10.1097/BS9.0000000000000069
Xiaoqian Lv, Yuting Hu, Lina Wang, Dongyue Zhang, Hao Wang, Yibo Dai, Xiaoxi Cui, Guoguang Zheng
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Abstract

Interleukin 34 (IL-34) is a cytokine that shares the receptor with colony-stimulating factor 1 (CSF-1). IL-34 is involved in a broad range of pathologic processes including cancer. We previously demonstrated that IL-34 promoted the proliferation and colony formation of human acute monocytic leukemia (AMoL) cells. However, the mechanism has not been elucidated. Here, by analyzing the gene profiles of Molm13 and THP1 cells overexpressing IL-34 (Molm13-IL-34 and THP1-IL-34), upregulation of the DNA damage-inducible transcript 4 (DDIT4) was detected in both series. Knockdown of DDIT4 effectively inhibited the proliferation, promoted apoptosis and colony formation in Molm13-IL-34 and THP1-IL-34 cells. Our results suggest that DDIT4 mediates the proliferation-promotive effect of IL-34 whereas does not mediate the promotive effect of IL-34 on colony formation in AMoL cells.

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DDIT4介导IL-34对人单核细胞白血病细胞增殖的促进作用
摘要白细胞介素34(IL-34)是一种与集落刺激因子1(CSF-1)共受体的细胞因子。IL-34参与广泛的病理过程,包括癌症。我们先前证明IL-34促进人类急性单核细胞白血病(AMoL)细胞的增殖和集落形成。然而,其机制尚未阐明。在此,通过分析过表达IL-34的Molm13和THP1细胞(Molm13-IL-34和THP1-IL-34)的基因图谱,在两个系列中都检测到DNA损伤诱导型转录物4(DDIT4)的上调。敲除DDIT4可有效抑制Molm13-IL-34和THP1-IL-34细胞的增殖,促进细胞凋亡和集落形成。我们的结果表明,DDIT4介导IL-34对AMoL细胞中集落形成的增殖促进作用,而不介导IL-4对集落形成形成的促进作用。
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