贝卡林通过抑制Notch1/NF-κB信号通路来对抗前列腺癌干细胞
Ming-Hui Wu1, Kun Wu1, Yuan-Bing Zhu2
1Department of Urology, Hubei University of Traditional Chinese Medicine, Wuhan, 430065, China.
Chinese journal of integrative medicine
|June 25, 2023
概括
拜卡林通过向Notch1/NF-κB途径,有效地抑制前列腺癌 (PCa) 的进展,减少癌症干细胞和促进亡在体内和体外模型中.
科学领域:
- 在瘤学瘤学.
- 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:
- 前列腺癌 (PCa) 仍然是一个重大的健康问题.
- 癌症干细胞 (CSCs) 在PCa进展和治疗耐药性方面发挥着至关重要的作用.
- 确定针对PCa干性的新型治疗剂是必不可少的.
研究的目的:
- 阐明贝卡林抗PCa作用的分子机制.
- 在体内和体外研究贝卡林对前列腺癌干细胞 (PCSC) 的影响.
- 确定Notch1/NF-κB途径在贝卡林治疗作用中的作用.
主要方法:
- 在裸体小鼠中的异种移植瘤模型被用baicalin治疗.
- 在体外研究中,使用PC3 PCSC治疗了baicalin.
- 分子分析包括RT-PCR,西部斑点,免疫光学,流细胞计和Transwell测定.
- 使用Notch1过度表达来评估途径的参与.
主要成果:
- 贝卡林在体内显著降低了瘤体积和体重.
- 贝卡林抑制了PCSC的增殖,迁移和入侵,同时在体外诱导了细胞灭绝.
- 贝卡林降低了关键的干度标志物 (ALDH1,CD44,CD133) 和Notch1的表达.
- 观察到Notch1/NF-κB通路的抑制,并且Notch1过度表达逆转了baicalin的作用.
结论:
- 贝卡林证明了对前列腺癌的治疗潜力.
- 拜卡林通过抑制Notch1/NF-κB信号通路来发挥其作用.
- 贝卡林有效地抑制了PCa的生长和进展.
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