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丙泊酚通过调节S100A4表达抑制EC-1细胞在体外的侵袭、血管生成和存活。

Propofol suppresses invasion, angiogenesis and survival of EC-1 cells in vitro by regulation of S100A4 expression.

作者信息

Guo X-G, Wang S, Xu Y-B, Zhuang J

机构信息

Department of Anesthesia, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangzhou, Guangdong, China.

出版信息

Eur Rev Med Pharmacol Sci. 2015 Dec;19(24):4858-65.

Abstract

OBJECTIVE

Propofol possess anticancer properties in several cancers. In the present study, we investigate the effect of propofol on the human esophageal squamous cell carcinomas (ESCC) EC-1 cells in vitro and its molecular mechanisms of action.

MATERIALS AND METHODS

EC-1 cells were explored to 10-100 μmol/L propofol for 72 h or 100 μmol/L/mL propofol for 24-72 h. EC-1 cells were explored to 100 μmol/L propofol for 24 h, then was transiently transfected into PcDNA3.1-S100A4 cDNA or PcDNA3.1 plasmid for 48 hrs. MTT, TUNEL, ELISA, migration, tube formation and immunoblotting were analized.

RESULTS

Propofol inhibits invasion, angiogenesis, proliferation and induces apoptosis in a dose and time-dependence manner, followed by deseased S100A4 expression by Western blot assay. Pre-transfection of PcDNA3.1-S100A4 cDNA inhibits propofol-induced apoptosis and promotes invasion and angiogenesis in EC-1 cells in vitro.

CONCLUSIONS

Propofol inhibited invasion, angiogenesis and induces apoptosis of human EC-1 cells in vitro through regulation of S100A4 expression. It not only can be an anesthesia agent, but also plays a important role of inhibiting the migration and angiogenesis of ESCC cells in the therapy of ESCC patients.

摘要

目的

丙泊酚在多种癌症中具有抗癌特性。在本研究中,我们调查丙泊酚对人食管鳞状细胞癌(ESCC)EC-1细胞的体外作用及其分子作用机制。

材料与方法

将EC-1细胞用10 - 100μmol/L丙泊酚处理72小时或用100μmol/L丙泊酚处理24 - 72小时。将EC-1细胞用100μmol/L丙泊酚处理24小时,然后瞬时转染PcDNA3.1 - S100A4 cDNA或PcDNA3.1质粒48小时。分析MTT、TUNEL、ELISA、迁移、管形成和免疫印迹。

结果

丙泊酚以剂量和时间依赖性方式抑制侵袭、血管生成、增殖并诱导凋亡,随后通过蛋白质印迹分析显示S100A4表达降低。预先转染PcDNA3.1 - S100A4 cDNA可抑制丙泊酚诱导的凋亡,并促进体外EC-1细胞的侵袭和血管生成。

结论

丙泊酚通过调节S100A4表达在体外抑制人EC-1细胞的侵袭、血管生成并诱导凋亡。它不仅可以作为一种麻醉剂,而且在ESCC患者的治疗中在抑制ESCC细胞的迁移和血管生成方面发挥重要作用。

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