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乳腺癌干细胞通过Akt/Sox2信号通路死亡

Seung-Yeon Ko^1,2, Seonghee Park¹, Youn-Hee Choi^1,2

¹Department of Physiology, College of Medicine, Ewha Womans University, Seoul 07804, Republic of Korea.

International journal of molecular sciences

|March 13, 2025

概括

原甲基 (PCA) 通过向Akt和Sox2通路,有效抑制乳腺癌生长和干细胞特性. 这种天然化合物对开发新的乳腺癌疗法充满希望.

科学领域:

在瘤学瘤学.
药理学药理学是指药理学的学科.
生物化学生化学

背景情况:

三重阴性乳腺癌 (TNBC) 由于其异质性,缺乏向疗法,以及乳腺癌干细胞 (BCSCs) 在复发和治疗耐药性方面的突出作用而构成重大临床挑战.
现有的乳腺癌治疗方法,包括荷尔蒙和向疗法,往往不足,导致持续的早期和晚期复发,突出显示需要新的治疗策略.
乳腺癌干细胞 (BCSCs) 是瘤发作,转移和治疗耐药性的关键驱动因素,使他们成为有效治疗乳腺癌的关键目标.

研究的目的:

为了研究原甲 (PCA) 的抗癌作用,这是一个来自 * Artemisia princeps * 的生物活性化合物,特别是对乳腺癌干细胞 (BCSCs).
阐明PCA对BCSCs作用的分子机制,重点关注关键信号通路和干细胞标记物.
评估PCA在乳腺癌临床前小鼠模型中的治疗潜力.

主要方法:

评估了PCA对乳腺癌细胞增殖和乳腺球形成的 in vitro 影响.
在PCA治疗后,通过CD44+/CD24-和化脱酶1A (ALDH1A) 表达来识别的BCSCs比例的量化变化.
在用PCA治疗的乳腺CSC中测量了Akt,酸化Akt (pAkt) 和Sox2的蛋白质水平.
在4T1乳腺癌小鼠模型中通过测量瘤体积和体重来评估PCA的体内疗效.

主要成果:

PCA证明了剂量依赖的抑制乳腺癌细胞生长和乳腺球的形成.
PCA治疗显著减少了表达CD44+/CD24和ALDH1A的群体,这表明BCSC分数下降.
PCA降低了乳房CSC中的Akt,pAkt和Sox2的蛋白质水平.
在体内研究表明,PCA的使用可降低4T1瘤的小鼠的瘤体积和体重.

结论:

甲基甲对乳腺癌具有显著的抗瘤活性,特别是通过向乳腺癌干细胞.
通过对Akt/pAkt和Sox2信号通路的下调调节,PCA的抗癌作用得到了调节.
对于乳腺癌的新型治疗策略的开发,PCA代表了一个有前途的天然化合物,特别是在克服与BCSCs相关的复发和耐药性方面.

关键词:

这就是ALDH1A.标签: 活动活动活动这就是Sox2x2的意思.乳腺癌乳腺癌乳腺癌癌症干细胞是一种癌症干细胞.原始甲 (protocatechualdehyde) 是一种甲.

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