TNF-α可促进原发性白血病细胞TGF-β1对Gli2表达的抑制作用。

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-02-22 DOI:10.1080/10799893.2021.1881555
Zhe Li, Shudan Mao, Ning Zhang
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引用次数: 0

摘要

目的:Hedgehog (Hh)信号通路调控包括白血病在内的多种肿瘤相关疾病。在原发性白血病细胞中,TNF-α是否促进TGF-β1对Gli2表达的抑制尚不明确。方法:用不同浓度的TGF-β1、TNF-α和SIS3治疗原发性白血病细胞。采用实时荧光定量PCR和western blot检测Gli2的表达。结果:我们发现TGF-β显著降低了Gli2的表达,与TNF-α联合治疗进一步降低了原发性白血病细胞中Gli2的表达。TNF-α可增加原发性白血病细胞中TGF-β ri和TGF-β rii蛋白的表达,而SIS3可抑制TGF-β的作用。结论:原发性白血病细胞中Gli2的表达受TGF-β的诱导,其表达依赖于smad3,且不依赖于Hh受体信号。
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Inhibition of TGF-β1 on Gli2 expression was promoted by TNF-α in primary leukemia cells.

Purpose: Hedgehog (Hh) signaling pathway regulates a variety of tumors-related diseases including leukemia. Whether inhibition of TGF-β1 on Gli2 expression is promoted by TNF-α in primary leukemia cells remains to be determined.

Methods: Primary leukemia cells were treated with TGF-β1, TNF-α or SIS3 at different concentrations. Gli2 expression was detected by quantitative real-time PCR and western blot analyses.

Results: We found that TGF-β significantly decreased Gli2 expression, and co-treatment with TNF-αfurther decreased Gli2 expression in primary leukemia cells. TNF-α can increased TGF-βRI and TGF-βRII protein expression in primary leukemia cells, while SIS3 inhibited the effect of TGF-β.

Conclusion: Our results suggest that Gli2 expression in primary leukemia cells is induced by TGF-β in a Smad3-dependent manner, and independent of Hh receptor signaling.

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来源期刊
Journal of Receptors and Signal Transduction
Journal of Receptors and Signal Transduction 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Journal of Receptors and Signal Tranduction is included in the following abstracting and indexing services: BIOBASE; Biochemistry and Biophysics Citation Index; Biological Abstracts; BIOSIS Full Coverage Shared; BIOSIS Previews; Biotechnology Abstracts; Current Contents/Life Sciences; Derwent Chimera; Derwent Drug File; EMBASE; EMBIOLOGY; Journal Citation Reports/ Science Edition; PubMed/MedLine; Science Citation Index; SciSearch; SCOPUS; SIIC.
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