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丙泊酚通过抑制肝母细胞瘤中CCL18的表达来抑制细胞进展。

Propofol Suppresses Cell Progression by Inhibiting CCL18 Expression in Hepatoblastoma.

作者信息

Zhang Hua, Lin Pingling, Fu Lei, Li Zhijun, Ding Yan

机构信息

Department of Pharmacy, Yantaishan Hospital, Yantai 264000, China.

Department of Pediatrics (I), Jiyang People's Hospital, Jinan 251400, China.

出版信息

J Oncol. 2021 Jul 26;2021:6880473. doi: 10.1155/2021/6880473. eCollection 2021.

Abstract

BACKGROUND

Propofol is an anesthetic commonly used clinically and has been found to have antitumor activity in various cancers. The purpose of this study was to investigate the role of propofol in hepatoblastoma (HB).

METHODS

CCK-8 and transwell were used to measure cell proliferation, migration, and invasion in HB cells. Cell apoptosis rate was measured by FCM. The expression of CCL18 in HB tissues and cells was detected by RT-qPCR. Western blotting was used to explore the protein expression of CCK18- and PI3K/AKT-related proteins.

RESULTS

The expression of CCL18 in HB tissues and cells was overexpressed compared with control groups. CCL18 knockdown was found to notably block cell proliferation and progression, while enhancing cell apoptosis in HuH-6 and HepT1 cells. Furthermore, propofol suppressed the proliferation of HB cells in a dose-dependent manner. According to the results, we chose 5 g/mL of propofol-treated cells for 48 hours as the subsequent experimental conditions. We found that propofol (5 g/mL, 48 h) significantly blocked cell migration and invasion, but induced cell apoptosis in HuH-6 and HepT1 cells. In addition, CCK18 overexpression facilitated cell progression in HB cells, while propofol dramatically suppressed the effect of CCK18. Besides that, propofol suppressed the PI3K/AKT pathway.

CONCLUSION

Propofol suppressed the development of HB cells by inhibiting CCK18 expression and the PI3K/AKT pathway. Therefore, we infer that propofol plays a role in the treatment of HB.

摘要

背景

丙泊酚是临床上常用的一种麻醉剂,已发现在多种癌症中具有抗肿瘤活性。本研究的目的是探讨丙泊酚在肝母细胞瘤(HB)中的作用。

方法

采用CCK-8和Transwell实验检测HB细胞的增殖、迁移和侵袭能力。通过流式细胞术检测细胞凋亡率。采用RT-qPCR检测HB组织和细胞中CCL18的表达。运用蛋白质免疫印迹法探究CCK18及PI3K/AKT相关蛋白的表达情况。

结果

与对照组相比,HB组织和细胞中CCL18的表达上调。发现敲低CCL18可显著抑制HuH-6和HepT1细胞的增殖和进展,同时增强细胞凋亡。此外,丙泊酚以剂量依赖的方式抑制HB细胞的增殖。根据结果,我们选择5μg/mL丙泊酚处理细胞48小时作为后续实验条件。我们发现丙泊酚(5μg/mL,48小时)显著阻断HuH-6和HepT1细胞的迁移和侵袭,但诱导细胞凋亡。此外,CCK18过表达促进HB细胞的进展,而丙泊酚显著抑制CCK18的作用。除此之外,丙泊酚抑制PI3K/AKT通路。

结论

丙泊酚通过抑制CCK18表达和PI3K/AKT通路抑制HB细胞的发展。因此,我们推断丙泊酚在HB的治疗中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e787/8331318/7f9e0004079b/JO2021-6880473.001.jpg

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