赛可沙尼D调节MDA-MB-231细胞中的STAT3和c-Myc表达:一个全面的体和体外研究.
Bhuvaneshwari Deivendran1, Suryaa Manoharan1, Ekambaram Perumal2
1Molecular Toxicology Laboratory, Department of Biotechnology, Bharathiar University, Coimbatore, 641046, India.
Applied biochemistry and biotechnology
|October 14, 2025
概括
赛可沙尼D (SSD) 显示出对三阴性乳腺癌 (TNBC) 的治疗潜力. 在临床前研究中,这种化合物有效抑制STAT3/c-Myc通路,降低癌细胞活力和迁移.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 三阴性乳腺癌 (TNBC) 是一种具有有限治疗选择的侵袭性亚型.
- 转录3 (STAT3) /c-Myc通路的信号转换器和激活器在TNBC中经常受到失调.
- 来自Bupleurum chinense的赛科沙尼D (SSD) 是一种潜在的抗癌剂.
研究的目的:
- 调查赛可沙尼D (SSD) 对三阴性乳腺癌 (TNBC) 的治疗潜力.
- 评估SSD对MDA-MB-231细胞中的STAT3/c-Myc信号通路的影响.
- 通过in silico和in vitro分析探索SSD的作用机制.
主要方法:
- 在接和分子动力学模拟中预测SSD-蛋白相互作用.
- 在体外测试包括细胞活力,增殖,迁移和亡.
- 基因表达分析和西式涂抹以评估途径调制.
主要成果:
- SSD 显示出对STAT3和c-Myc的显著结合亲和力.
- 在体外,SSD降低了MDA-MB-231细胞活力 (IC50 7.293 μM),增殖和迁移.
- SSD诱导了亡,改变了细胞形态,并依剂量抑制了STAT3酸化和c-Myc表达.
结论:
- 赛可沙尼D对TNBC具有有前途的治疗潜力.
- SSD有效地准了STAT3/c-Myc通路,提供了一个新的治疗策略.
- 这些发现支持进一步研究SSD用于TNBC治疗的临床开发.
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