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安德罗格拉福利德通过抑制DKK1表达来使质瘤对temozolomide敏感

Zhan-Sheng Zhang^1,2, Zi-Xuan Gao^1,2, Jin-Jin He¹

¹Department of Pharmacy, The First Afffliated Hospital of Henan University, N. Jinming Ave, Kaifeng, 475004, China.

British journal of cancer

|September 12, 2024

概括

安德罗格拉福利德通过抑制DKK1表达来增强泰莫佐洛米德 (TMZ) 在质瘤治疗中的疗效. 这种组合疗法在临床前模型中改善了抗瘤效应和存活率.

科学领域:

神经瘤学神经瘤学
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

泰莫佐洛米德 (Temozolomide,简称TMZ) 是用于质瘤的第一线化疗,但其临床疗效有限.
迫切需要新的策略来克服质瘤患者的TMZ耐药性.

研究的目的:

调查DKK1在TMZ介导的质瘤进展中的作用.
评估andrographolide (AND) 作为在质瘤治疗中对TMZ的敏感剂.

主要方法:

西部斑块,qRT-PCR和免疫组织化学分析DKK1表达.
在体内研究中,使用 ортотоп性质瘤模型来评估瘤生长和存活率.
在HPLC测定andrographolide的血脑屏障透率.

主要成果:

TMZ治疗增加了DKK1在质瘤细胞和瘤中的表达,促进了扩散.
安德罗格拉福利德通过向EGFR下游通路 (MEK-ERK,PI3K-Akt) 来抑制TMZ诱导的DKK1表达.
结合TMZ和andrographolide在临床前质瘤模型中显示出增强的抗瘤活性和改善的存活率.

结论:

安德罗格拉福利德增强了temozolomide对质瘤的抗瘤活性.
抑制DKK1的表达是一种关键的机制,andrographolide使质瘤细胞对TMZ敏感.

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