| 摘要: |
| 目的 观察香芹酚对前列腺癌细胞增殖、凋亡以及侵袭的影响，并从丝裂原活化蛋白激酶（mitogen-activated protein kinase，MAPK）信号通路探讨其可能的作用机制。方法 采用80 μmol/L浓度的香芹酚干预前列腺癌DU145细胞（香芹酚组）24 h或者48 h，同时设置不加香芹酚的阴性对照组。CCK-8法检测细胞在第0、1、2、3、4、5天的生长情况，绘制细胞生长曲线；流式细胞术检测细胞凋亡情况；Transwell侵袭实验检测细胞侵袭能力；RT-PCR以及蛋白质印迹分析检测基质金属蛋白酶9（MMP-9）及其抑制剂TIMP-1的表达；蛋白质印迹分析检测聚腺苷二磷酸核糖聚合酶（PARP）、半胱天冬氨酸蛋白酶9（caspase-9）的表达以及细胞外信号调节激酶（ERK）、p38信号通路的激活情况。结果 与阴性对照组比较，香芹酚作用后前列腺癌细胞DU145活性明显受到抑制，作用的第3天起细胞增殖能力降低（P<0.05，P<0.01）。香芹酚作用后，细胞凋亡率升高（P<0.05），细胞侵袭能力降低（P<0.01），细胞TIMP-1、caspase-9表达升高，PARP发生裂解，p38信号被激活，同时MMP-2表达降低，ERK信号通路受到抑制。结论 香芹酚能够抑制前列腺癌细胞的增殖和侵袭，诱导其凋亡，其作用与MAPK信号通路有关。 |
| 关键词: 香芹酚 前列腺肿瘤 细胞增殖 细胞凋亡 肿瘤侵润 丝裂原活化蛋白激酶类 |
| DOI：10.3724/SP.J.1008.2014.00285 |
| 投稿时间：2013-09-05修订日期：2013-10-14 |
| 基金项目:辽宁省博士科研启动基金（20101060）. |
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| Anti-prostate cancer effect of carvacrol via MAPK signaling pathway |
| LI Gang,MU Zhong-yi,HUANG Yan,FU Cheng* |
(Department of Urinary Surgery, Liaoning Cancer Hospital & Institute, Shenyang 110042, Liaoning, China
*Corresponding author.) |
| Abstract: |
| Objective To investigate the effects of carvacrol on proliferation, apoptosis and invasion of human prostate cancer cells in vitro, and to explore the role of mitogen-activated protein kinase (MAPK) signaling pathway in the related mechanism. Methods Prostate cancer cells DU145 were treated with (carvacrol group) or without (negative control group) 80 μmol/L carvacrol for 24 or 48 hours. CCK-8 assay and cell growth curve were used to detect the proliferation of DU145 cells on day 0, 1, 2, 3, 4 and 5. Cell apoptosis and invasion were assessed by FACS method and transwell assay, respetively. RT-PCR and Western blotting analysis were used to detect the expression of matrix metalloproteinase 9 (MMP-9) and its inhibitor TIMP-1. Expressions of poly(ADP)-ribose polymerase (PARP), caspase-9, and activation of extracellular signal-regulated kinase (ERK) and p38 were also detected by Western blotting analysis. Results Compared with negative control group, cell viability was inhibited in the carvacrol group and cell proliferation was decreased significantly on the third day of treatment(P<0.05, P<0.01). Apoptosis rate of DU145 cells was significantly increased (P<0.05) and the invasion capability of DU145 cells was significantly decreased in the carvacrol group (P<0.01). Expressions of TIMP-1 and caspase-9 were increased in the carvacrol group, with fragmented PRAP, activated p38 signaling pathway, and inhibited MMP-2 activity of ERK signaling pathway. Conclusion Carvacrol can inhibit cell growth, invasion and induce apoptosis of DU145 cells, which involves MAPK signaling pathway. |
| Key words: carvacrol prostatic neoplasms cell proliferation apoptosis neoplasm invasiveness mitogen-activated protein kinases |
