丙泊酚抑制脑胶质瘤 U87 细胞增殖和侵袭的机制及其对 miR-134 表达的影响。
Mechanisms for propofol in inhibiting the proliferation and invasion of glioma U87 cells and its effect on miR-134 expression.
机构信息
Department of Anesthesiology, Hengshui People's Hospital, Hengshui Hebei 053000, China.
出版信息
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2021 Jan 28;46(1):18-24. doi: 10.11817/j.issn.1672-7347.2021.190734.
OBJECTIVES
To investigate the effects of propofol on the proliferation and invasion of glioma U87 cells and to explore the possible anti-tumor mechanisms.
METHODS
The glioma U87 cells was divided into a blank group, a positive control group, and the propofol groups (1.00, 2.00 or 5.00 mmol/L). Cell counting kit-8 (CCK-8) was used to detect cell proliferation; Transwell method was used to detect the effect of propofol on invasion and migration of U87 cells; real-time PCR was used to detect the expression of microRNA-134 (miR-134); Western blotting was used to detect the expression levels of reproduction-related protein Ki-67, invasion-related protein metalloproteinase-2 (MMP-2), metalloproteinase-9 (MMP-9) and phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) signaling pathway-related protein.
RESULTS
Compared with the blank group, the proliferation, invasion and migration capacity of U87 cells were reduced in the positive control group and the propofol groups after 48 hours (all <0.05), along with the decreased expression of Ki-67, MMP-2 and MMP-9 and the ratio of p-PI3K/PI3K and p-Akt/Akt (all <0.05), while the level of miR-134 was increased significantly (<0.05). Compared with the positive control group and the 1.00 mmol/L propofol-treated group, the proliferation, invasion and migration capacity of U87 cells, the expression of Ki-67, MMP-2 and MMP-9, and the ratio of p-PI3K/PI3K and p-Akt/Akt was decreased significantly after 48 hours (all <0.05), while the level of miR-134 was increased significantly in the 2.00 and 5.00 mmol/L propofol-treated groups (both <0.05). Compared with the 2.00 mmol/L propofol-treated group, the proliferation, invasion and migration capacity of U87 cells, the expression of Ki-67, MMP-2 and MMP-9, and the ratio of p-PI3K/PI3K and p-Akt/Akt was decreased significantly after 48 hours in the 5.00 mmol/L propofol-treated group (all <0.05), while the level of miR-134 was increased significantly (<0.05).
CONCLUSIONS
Propofol can decrease the proliferation rate, and the invasion and migration abilities of U87 cells, which may be achieved by up-regulation of miR-134 and suppression of PI3K/Akt signaling pathway.
目的
研究丙泊酚对脑胶质瘤 U87 细胞增殖和侵袭的影响，并探讨其可能的抗肿瘤机制。
方法
将脑胶质瘤 U87 细胞分为空白组、阳性对照组和丙泊酚组（1.00、2.00 或 5.00mmol/L）。采用细胞计数试剂盒-8（CCK-8）检测细胞增殖；Transwell 法检测丙泊酚对 U87 细胞侵袭和迁移的影响；实时 PCR 检测微小 RNA-134（miR-134）的表达；Western blot 检测增殖相关蛋白 Ki-67、侵袭相关蛋白基质金属蛋白酶-2（MMP-2）、基质金属蛋白酶-9（MMP-9）和磷脂酰肌醇 3 激酶（PI3K）/蛋白激酶 B（Akt）信号通路相关蛋白的表达水平。
结果
与空白组比较，48h 时阳性对照组和丙泊酚组 U87 细胞增殖、侵袭和迁移能力均降低（均<0.05），Ki-67、MMP-2 和 MMP-9 表达降低（均<0.05），p-PI3K/PI3K 和 p-Akt/Akt 比值降低（均<0.05），miR-134 水平明显升高（均<0.05）。与阳性对照组和 1.00mmol/L 丙泊酚组比较，48h 时 2.00、5.00mmol/L 丙泊酚组 U87 细胞增殖、侵袭和迁移能力降低（均<0.05），Ki-67、MMP-2 和 MMP-9 表达降低（均<0.05），p-PI3K/PI3K 和 p-Akt/Akt 比值降低（均<0.05），miR-134 水平升高（均<0.05）。与 2.00mmol/L 丙泊酚组比较，5.00mmol/L 丙泊酚组 U87 细胞增殖、侵袭和迁移能力降低（均<0.05），Ki-67、MMP-2 和 MMP-9 表达降低（均<0.05），p-PI3K/PI3K 和 p-Akt/Akt 比值降低（均<0.05），miR-134 水平升高（均<0.05）。
结论
丙泊酚可降低 U87 细胞的增殖率及侵袭和迁移能力，其机制可能与上调 miR-134 表达和抑制 PI3K/Akt 信号通路有关。
Zotero 插件