免费
Eugenol通过HER2/PI3K-AKT途径诱导的细胞凋亡和S期停滞减轻了乳腺癌癌性病变。
Oncotarget. 2017 Aug 22 ;8(34):56296-56310. Epub 2017 May 5. PMID: 28915591
最小马
丁香醇可以与丁香芽的油提取物分离,并且具有许多药理功能,例如抗癌和透皮吸收。 HER2/PI3K-AKT是乳腺癌发展的关键信号通路。在这项研究中,80μm的丁醇可以显着抑制HER-2阳性MCF-10AT细胞的增殖,并且抑制速率高达32.8%,但对MCF-7和MCF-10A细胞没有明显的抑制作用,而HER2弱表达较弱。丁香酚还显着诱导了人类乳腺癌病变MCF-10ATCELS细胞凋亡和细胞周期S期停滞,但通过转染PCDNA3.1-HER2,生物学作用在HER2过表达后几乎消失。 In MCF-10AT cells treated by 180 μM eugenol, the protein expressions of HER2, AKT, PDK1, p85, Bcl2, NF-κB, Bad and Cyclin D1 were decreased andthe decreased rates were respectively 63.0%, 60.0%, 52.9%, 62.9%, 37.1%, 47.2%, 61.7%, 59.1%, while the P21,P27和BAX表达分别增加了4.48-,4.76和2.57倍。在大鼠乳腺癌病变的大鼠模型中,用于外部使用的1 mg丁香醇显着抑制乳腺癌病变的进展,乳腺癌病变的发生率和侵入性癌的发生率降低了约30.5%。此外,外部(1 mg)的丁香酚显着降低了HER2(62.9%),AKT(58.6%),PDK1(56.4%),p85(54.3%),BCL2(59.3%),NF-κB(65.7%),BAD(65.7%),p21(64.0%),P21(44.0%),PDK1(54.3%),pdk1(54.3%),p21(44.0%),PDK1(54.3%),p21(44.0%和P2),pdk1(54.3%),pdk1(54.3%),p21(44.0%和P2),pdk1(54.3%),pdk1(54.3%),cyclin d1(43.), Bax蛋白表达分别增加了1.83-,2.52-和2.51倍。结果表明,丁香酚可以通过阻止HER2/PI3K-AKT信号网络来显着抑制乳腺癌病变的发展。因此,尤格诺醇可能是乳腺癌病变的有前途的外部药物。