大黄素抑制维罗非尼耐药黑色素瘤细胞增殖
Emodin Inhibits Proliferation of Vemurafenib-resistant Melanoma Cells
黄伟 1胡中柱 2张雅琪 3罗云蔓3
作者信息
- 1. 黄冈市中心医院骨科,湖北黄冈 438000
- 2. 黄冈市中心医院皮肤科,湖北黄冈 438000
- 3. 黄冈市中心医院肿瘤科,湖北黄冈 438000
- 折叠
摘要
目的 探讨大黄素对维罗非尼耐药黑色素瘤细胞(A375R)的体外抑制作用.方法 分别用0、80、160、320 μmol·L-1的大黄素处理对照组和A—C组细胞48 h.分别通过CCK-8法、流式细胞术和蛋白免疫印迹检测大黄素对各组细胞增殖、凋亡和PI3K/AKT/mTOR信号通路关键蛋白(Bcl-2、Akt、p-Akt、mTOR、p-mTOR)表达的影响.结果 与对照组相比,大黄素处理后的A—C组细胞增殖抑制率和凋亡率均显著提高(P＜0.01和P＜0.05),且作用呈现浓度依赖性;A—C组细胞Bcl-2蛋白的表达水平均明显降低(P＜0.05),p-Akt及p-mTOR蛋白的表达均下降,其中B、C组与对照组比较差异有统计学意义(P＜0.05).结论 大黄素可抑制A375R细胞增殖并诱导其凋亡,其机制可能与抑制PI3K/AKT/mTOR信号通路的活性有关.
Abstract
Objective To investigate the in vitro inhibitory effect of emodin on vemurafenib-re-sistant melanoma cells(A375R).Methods A375R cells in Control Group and Group A-C were treated with 0,80,160,and 320 μmol·L-1 emodin for 48 h.The effects of emodin on cell prolifer-ation,apoptosis and the expression of key proteins(Bcl-2,Akt,p-Akt,mTOR,p-mTOR)of PI3K/AKT/mTOR signaling pathway were detected by CCK-8 assay,flow cytometry and western blot-ting in the groups,respectively.Results Compared with Control Group,the cell proliferation inhi-bition and apoptosis rates were significantly increased in a concentration-dependent manner in emodin-treated Group A-C(P＜0.01 and P＜0.05,respectively).The expression levels of Bcl-2 protein in the cells of Groups A-C were significantly reduced(P＜0.05),and the expression levels of p-Akt and p-mTOR proteins were decreased,of which the differences between Groups B and C and Control group were statistically significant(P＜0.05).Conclusion Emodin can inhibit prolif-eration and induce apoptosis in vemurafenib-resistant melanoma A375R cell by a mechanism that may be related to the inhibition of PI3K/AKT/mTOR signaling pathway.
关键词
维罗非尼/恶性黑色素瘤/大黄素/PI3K/AKT/mTORKey words
vemurafenib/malignant melanoma/emodin/PI3K/AKT/mTOR引用本文复制引用
基金项目
湖北省卫生健康科研基金资助项目(WJ2021Q016)
出版年
2024
NETL
NSTL
万方数据