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MiR-20a-5p suppressed TGF-β1-triggered apoptosis of human bronchial epithelial BEAS-2B cells by targeting STAT3.
Molecular and Cellular Probes ( IF 3.3 ) Pub Date : 2019-12-25 , DOI: 10.1016/j.mcp.2019.101499
Xiuyun Lv 1 , Lihong Wang 1 , Tianji Zhu 1
Affiliation  

Apoptosis of bronchial epithelial cells contributes to lung diseases, including asthma. Although miR-20a-5p is reportedly downregulated in the bronchial epithelia of asthmatic patients, its function and mechanism still need to be explored. Here, we explored how miR-20a-5p affects human bronchial epithelial cells stimulated with transforming growth factor (TGF)-β1. Using qRT-PCR, we observed downregulated miR-20a-5p levels in these cells. After transfecting miR-20a-5p mimics or inhibitors into human bronchial epithelium BEAS-2B cells, a Cell Counting Kit-8 assay and flow cytometry analysis showed that the mimics mitigated suppression of cell viability and acceleration of apoptosis that was triggered by TGF-β1, whereas the inhibitors exerted the opposite effects. TGF-β1 induced a decrease in expression of Bcl-2 and an increase in expression of Bax, both of which were inhibited by miR-20a-5p mimics and further enhanced by miR-20a-5p inhibitors. Further study verified that miR-20a-5p targeted the signal transducer and activator of transcription 3 (STAT3) and the STAT3 level was inversely related to the miR-20a-5p level. Furthermore, STAT3 overexpression partly counteracted the miR-20a-5p-induced anti-apoptotic effect in TGF-β1-treated BEAS-2B cells. In summary, this study suggested that miR-20a-5p restrained apoptosis in TGF-β1-stimulated BEAS-2B cells by targeting STAT3. MiR-20a-5p thus may be a novel therapeutic target for asthma treatment.

中文翻译:

MiR-20a-5p通过靶向STAT3抑制TGF-β1触发的人支气管上皮BEAS-2B细胞凋亡。

支气管上皮细胞的凋亡导致包括哮喘在内的肺部疾病。尽管据报道在哮喘患者的支气管上皮细胞中miR-20a-5p被下调,但其功能和机制仍有待探索。在这里,我们探讨了miR-20a-5p如何影响转化生长因子(TGF)-β1刺激的人支气管上皮细胞。使用qRT-PCR,我们在这些细胞中观察到miR-20a-5p水平下调。将miR-20a-5p模拟物或抑制剂转染到人支气管上皮BEAS-2B细胞后,Cell Counting Kit-8分析和流式细胞仪分析表明,该模拟物减轻了由TGF-β1触发的细胞活力抑制和凋亡加速,而抑制剂发挥相反的作用。TGF-β1诱导Bcl-2的表达减少和Bax的表达增加,两者均被miR-20a-5p模拟物抑制,并被miR-20a-5p抑制剂进一步增强。进一步的研究证实,miR-20a-5p靶向信号转导和转录激活因子3(STAT3),且STAT3水平与miR-20a-5p水平成反比。此外,STAT3过表达部分抵消了TGF-β1处理的BEAS-2B细胞中miR-20a-5p诱导的抗凋亡作用。总之,这项研究表明,miR-20a-5p通过靶向STAT3来抑制TGF-β1刺激的BEAS-2B细胞凋亡。因此,MiR-20a-5p可能是哮喘治疗的新型治疗靶标。进一步的研究证实,miR-20a-5p靶向信号转导和转录激活因子3(STAT3),且STAT3水平与miR-20a-5p水平成反比。此外,STAT3过表达部分抵消了TGF-β1处理的BEAS-2B细胞中miR-20a-5p诱导的抗凋亡作用。总之,这项研究表明,miR-20a-5p通过靶向STAT3来抑制TGF-β1刺激的BEAS-2B细胞凋亡。因此,MiR-20a-5p可能是哮喘治疗的新型治疗靶标。进一步的研究证实,miR-20a-5p靶向信号转导和转录激活因子3(STAT3),且STAT3水平与miR-20a-5p水平成反比。此外,STAT3过表达部分抵消了TGF-β1处理的BEAS-2B细胞中miR-20a-5p诱导的抗凋亡作用。总之,这项研究表明,miR-20a-5p通过靶向STAT3来抑制TGF-β1刺激的BEAS-2B细胞凋亡。因此,MiR-20a-5p可能是哮喘治疗的新型治疗靶标。
更新日期:2019-12-25
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