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MicroRNA-125b exerts antitumor functions in cutaneous squamous cell carcinoma by targeting the STAT3 pathway
Cellular & Molecular Biology Letters ( IF 9.2 ) Pub Date : 2020-03-05 , DOI: 10.1186/s11658-020-00207-y
Ke Tian 1 , Wanggen Liu 2 , Jing Zhang 3 , Xiaoyi Fan 3 , Jingyuan Liu 3 , Nan Zhao 3 , Chunxia Yao 3 , Guoying Miao 1
Affiliation  

MicroRNA-125b (miR-125b) is downregulated in human cutaneous squamous cell carcinoma (CSCC). However, its function in CSCC has yet to be extensively explored. Here, we analyze the relationship between signal transducer and activator of transcription 3 (STAT3) and miR-125b in CSCC. Western blotting and quantitative RT-PCR were used to determine the expression of the miR-125b–STAT3 axis in human CSCC tissues and cell lines. The direct regulatory effect of miR-125b on STAT3 expression was assessed using a luciferase reporter gene assay and RNA immunoprecipitation assay. The MTT assay and flow cytometry were used to determine the role of the miR-125b–STAT3 axis in CSCC cell proliferation and apoptosis. MiR-125b expression levels were significantly lower in CSCC cell lines and tissues than in normal cell lines and tissues. STAT3 was identified as the direct target of miR-125b. Upregulation of miR-125b and downregulation of STAT3 suppressed cell proliferation and promoted cell apoptosis. Cyclin D1 and Bcl2 were identified as the downstream targets of the miR-125–STAT3 axis. Our findings indicate that miR-125b acts as a tumor suppressor in CSCC by targeting the STAT3 pathway. This observation increases our understanding of the molecular mechanisms of CSCC. Therapies aimed at activating miR-125b or inhibiting STAT3 signaling should be explored as potential treatments for CSCC.

中文翻译:

MicroRNA-125b 通过靶向 STAT3 通路在皮肤鳞状细胞癌中发挥抗肿瘤作用

MicroRNA-125b (miR-125b) 在人皮肤鳞状细胞癌 (CSCC) 中下调。然而,它在 CSCC 中的作用还有待广泛探索。在这里,我们分析了信号转导与转录激活因子 3 (STAT3) 和 miR-125b 在 CSCC 中的关系。Western印迹和定量RT-PCR用于确定人CSCC组织和细胞系中miR-125b-STAT3轴的表达。使用荧光素酶报告基因测定和 RNA 免疫沉淀测定评估 miR-125b 对 STAT3 表达的直接调节作用。MTT测定和流式细胞术用于确定miR-125b-STAT3轴在CSCC细胞增殖和凋亡中的作用。CSCC 细胞系和组织中的 MiR-125b 表达水平显着低于正常细胞系和组织。STAT3 被确定为 miR-125b 的直接靶标。miR-125b的上调和STAT3的下调抑制细胞增殖并促进细胞凋亡。Cyclin D1 和 Bcl2 被确定为 miR-125-STAT3 轴的下游靶标。我们的研究结果表明,miR-125b 通过靶向 STAT3 通路在 CSCC 中充当肿瘤抑制因子。这一观察增加了我们对 CSCC 分子机制的理解。应探索旨在激活 miR-125b 或抑制 STAT3 信号传导的疗法作为 CSCC 的潜在治疗方法。我们的研究结果表明,miR-125b 通过靶向 STAT3 通路在 CSCC 中充当肿瘤抑制因子。这一观察增加了我们对 CSCC 分子机制的理解。应探索旨在激活 miR-125b 或抑制 STAT3 信号传导的疗法作为 CSCC 的潜在治疗方法。我们的研究结果表明,miR-125b 通过靶向 STAT3 通路在 CSCC 中充当肿瘤抑制因子。这一观察增加了我们对 CSCC 分子机制的理解。应探索旨在激活 miR-125b 或抑制 STAT3 信号传导的疗法作为 CSCC 的潜在治疗方法。
更新日期:2020-03-05
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