滴氧基宁通过调节PI3K/AKT/mTOR通路来激活肝细胞癌细胞的自
Mengqing Ma1,2, Rui Hu3,1,2, Qi Huang3,1,2
1Department of Liver Disease, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, Guangdong, 518033, China.
Cancer cell international
|December 19, 2024
概括
滴氧基宁 (DIG) 通过通过PI3K/AKT/mTOR途径诱导自,有效抑制肝细胞癌 (HCC) 的进展. 这种天然化合物显示出作为一种新的,低毒性癌症治疗的前景.
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 生物化学
背景情况:
- 肝细胞癌 (HCC) 是一种高度恶性瘤,有效治疗方法有限.
- 目前针对HCC的向组合免疫疗法面临着不良影响和低响应率的挑战.
- 传统中医提供低毒性,成本效益高的抗癌药物.
研究的目的:
- 通过高通量表型查识别新型抗HCC药物.
- 调查狄戈西基宁 (DIG) 对HCC的治疗潜力和作用机制.
- 探索DIG对PI3K/AKT/mTOR信号通路和自的影响.
主要方法:
- 1,444种生物活性化合物的高通量表型选.
- 使用CCK8,乳酸脱酶和殖民地形成试验进行体外验证.
- 机械学研究包括传输电子显微镜,西式涂抹,免疫光学,网络药理学和分子对接.
- 在体内评估使用皮下异种移植瘤模型.
主要成果:
- 滴氧基宁 (DIG) 在体外显著阻碍了HCC细胞的进展和增殖.
- 通过诱导自,DIG被证明可以通过诱导自来抑制HCC细胞增殖.
- 网络药理学和分子对接表明,DIG针对PI3K/AKT/mTOR途径,并通过比较治疗证实了这一点.
- 在体内研究表明,DIG有效地阻止了皮下异种移植瘤的生长.
结论:
- 滴氧基宁 (DIG) 是肝细胞癌 (HCC) 的有前途的治疗药物.
- 通过调节PI3K/AKT/mTOR通路来诱导自,DIG发挥了它的抗HCC作用.
- 表型查加速了针对关键分子通路的新型HCC疗法的发现.
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