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特里普托利德通过通过ROCK/PTEN/Akt轴减轻上皮质-介质细胞过渡来减少MDA-MB-231细胞转移

Qinhang Wu¹, Xuejiao Leng¹, Xuelin Ma¹

¹School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, 210023, P.R. China.

Chemistry & biodiversity

|November 1, 2023

概括

一种天然化合物托利德 (Triptolide) 通过诱导亡和抑制上皮细胞-介质细胞过渡来抑制三阴性乳腺癌 (TNBC) 转移. 它针对ROCK1,为攻击性TNBC提供了潜在的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
自然产品化学化学

背景情况:

三阴性乳腺癌 (TNBC) 是一种具有攻击性的亚型,由于转移率高,预后不佳.
特里普托利德是一种天然的三氧化二二烯,具有潜在的抗瘤特性.
了解TNBC转移的机制对于开发有效的治疗方法至关重要.

研究的目的:

为了研究三胺对MDA-MB-231 TNBC细胞的转移性抑制作用.
阐明三托利德作用的潜在分子机制.
确定三胺作为TNBC的潜在治疗剂.

主要方法:

细胞增殖,细胞亡,迁移和入侵测定是在用triptolide治疗的MDA-MB-231细胞上进行的.
西方涂抹和qRT-PCR用于分析关键转移性标记物的蛋白质和mRNA表达水平 (ROCK1,p-Akt,N-cadherin,vimentin,MMP-9,PTEN,E-cadherin).
用Y27632进行了分子对接和ROCK1抑制研究,以确认目标.

主要成果:

在MDA-MB-231细胞中以剂量和时间依赖的方式抑制了triptolide的增殖和诱导了细胞亡.
低剂量托利德显著降低了MDA-MB-231细胞迁移和入侵.
特里普托利德调节了关键EMT标记物的表达,降低了ROCK1,p-Akt,N-cadherin,vimentin和MMP-9,同时增加了PTEN和E-cadherin. ROCK1被确定为主要目标.

结论:

托利德有效地抑制了MDA-MB-231 TNBC细胞的增殖,迁移和入侵.
特里普托利德通过诱导亡和通过ROCK1信号来抑制上皮细胞-介质细胞过渡 (EMT) 来发挥其抗转移作用.
特里普托利德是向转移性TNBC的有希望的治疗候选药物.

关键词:

在MDA-MB-231细胞中.在Rock1上,你会看到Rock1.灭症 (apoptosis) 是一种死亡的过程.转移转移转移转移自然化合物自然化合物

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