斯科帕龙通过NF-κB信号通路抑制乳腺癌细胞活力
Xiaoying Wu1, Xiaobo Li2, Jing Li2
1Mongolian Medical College, Inner Mongolia University for Nationalities, Tongliao, Inner Mongolia Autonomous Region 028000, P.R. China.
Experimental and therapeutic medicine
|June 22, 2023
概括
斯科帕龙 (SCO) 通过降低SNHG12/miR-140-3p/TRAF2轴的调节来抑制乳腺癌细胞活力,抑制NF-κB信号传递. 这项研究确定了SCO作为乳腺癌的潜在治疗剂.
科学领域:
- 药理学和分子生物学
- 在瘤学瘤学.
- 自然产品化学 自然产品化学
背景情况:
- 斯科帕龙 (SCO),来自Artemisia capillaris,具有不同的药理活动.
- 乳腺癌 (BC) 仍然是一个重大的全球健康挑战,需要新的治疗策略.
- 了解BC进展背后的分子机制对于有针对性的治疗开发至关重要.
研究的目的:
- 为了研究Scoparone (SCO) 在乳腺癌 (BC) 细胞中的抗癌潜力.
- 阐明SCO对BC细胞产生影响的分子机制.
- 探索长非编码RNA (lncRNA) SNHG12/microRNA (miRNA) 140-3p/TRAF2轴在SCO介导的BC抑制中的作用.
主要方法:
- 用细胞计数工具-8.8评估细胞活力.
- 通过流细胞计分析了亡.
- 使用RT-qPCR和西式斑点测量,量化了SNHG12,miR-140-3p和TRAF2的表达水平.
- 核细胞质分离确定了SNHG12的细胞局部.
- 评估了NF-κB信号通路的激活.
主要成果:
- SCO表现出时间和剂量依赖的BC细胞活力的抑制.
- 在BC细胞中,SCO抑制了上调 lncRNA SNHG12 的表达.
- SNHG12充当了竞争的内源RNA,使miR-140-3p变为海绵,并减少了它的表达.
- 由SCO引起的SNHG12下调导致TRAF2的表达和活性下降.
- 抑制TRAF2活性降低了NF-κB信号传递,降低了BC细胞活力和迁移,同时促进了细胞亡.
结论:
- 斯科帕龙有效地抑制乳腺癌细胞活力,并促进细胞亡.
- SCO通过准SNHG12/miR-140-3p/TRAF2轴来发挥其作用,从而抑制NF-κB信号通路.
- SCO代表了乳腺癌治疗的有前途的治疗候选药物,其机制为进一步研究提供了理论基础.
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