七氟烷抑制宣威肺癌XWLC-05细胞生物学行为

全宇航; 王忠慧; 李珊珊; 刘光顺

doi:10.12259/j.issn.2095-610X.S20211202

七氟烷抑制宣威肺癌XWLC-05细胞生物学行为

doi: 10.12259/j.issn.2095-610X.S20211202

昆明医科大学第三附属医院/云南省肿瘤医院麻醉科，云南昆明　650118

基金项目: 云南省科技厅-昆明医科大学应用基础研究联合专项基金资助项目（2018FE001-070；2019FE001-248）

详细信息

作者简介:
全宇航（1983～），男，河北唐山人，麻醉学硕士，主治医师，主要从事麻醉药物与肿瘤的临床及科研工作

通讯作者:
王忠慧，E-mail：skywz911@sina.com

中图分类号: R734.2;R730.2
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出版历程
- 收稿日期: 2021-10-05
- 网络出版日期: 2021-11-16
- 刊出日期: 2021-12-15

Sevoflurane Inhibits Xuanwei Lung Cancer Cell Line XWLC-05

Dept. of Anesthesiology ，The 3rd Affiliated Hospital of Kunming Medical University/Cancer Hospital of Yunnan Province，Kunming Yunnan 650118，China

摘要

摘要: 目的了解七氟烷对宣威肺癌细胞XWLC-05增殖、迁移、侵袭及恶性行为的影响，并进一步探讨其潜在机制。方法七氟烷对XWLC-05细胞进行处理，体外实验检测XWLC-05细胞增殖、凋亡、迁移和侵袭变化；体内实验检测XWLC-05细胞致瘤性，蛋白印迹法分析增殖关键分子PI3K/AKT、细胞侵袭蛋白MMP-2/MMP-9的表达。结果对照组的克隆形成数（287.5±23.1）个，高于实验组（174.1±16.3）个，（P < 0.05）；对照组的凋亡率（1.60±0.38）%，低于实验组（31.48±5.81）%，（P < 0.01）；对照组迁移细胞数（87.8±10.2）%，高于实验组（35.2±4.4）%，（P < 0.05）；对照组侵袭细胞数（93.6±7.3）个，高于实验组（30.7±3.2）个，（P < 0.01）。七氟烷处理下调增殖蛋白分子PI3K、p-AKT和侵袭蛋白分子MMP-2、MMP-9的表达水平（P < 0.05）。结论七氟烷通过抑制PI3K/AKT信号通路降低宣威肺癌细胞XWLC-05的增殖能力，诱导细胞凋亡，减弱XWLC-05细胞的迁移、侵袭和成瘤能力。七氟烷可能成为宣威肺癌治疗的一种新方法。
- 七氟烷 /
- 宣威肺癌 /
- 细胞凋亡 /
- 细胞增殖
Abstract: Objective To investigate the effects of sevoflurane on proliferation, migration, invasion and malignant behavior of Xuanwei lung cancer cells XWLC-05, and to further explore its potential mechanism. Method XWLC-05 cells were treated with sevoflurane, and the changes of proliferation, apoptosis, migration and invasion of XWLC-05 cells were detected in vitro; the tumorigenicity of XWLC-05 cells was detected in vivo, and the expressions of PI3K/AKT and MMP-2 / MMP-9 were analyzed by Western blot. Result The number of clones in control group （287.5±23.1） was higher than that in experimental group （174.1±16.3）（P < 0.05）; the apoptosis rate in the control group （1.60±0.38） was significantly lower than that in the experimental group （31.48±5.81）（P < 0.01）, and the number of migrating cells in the control group （87.8±10.2） was significantly higher than that in the experimental group （35.2±4.4）（P < 0.05）. The number of invasive cells in the control group（93.6±7.3） was significantly higher than that in the experimental group （30.7±3.2）（P < 0.01）. Sevoflurane treatment significantly decreased the expression levels of PI3K, p-Akt and MMP-2, MMP-9 （P < 0.05）. Conclusion By inhibiting PI3K/AKT signaling pathway, sevoflurane decreased the proliferation ability of XWLC-05, induced apoptosis, and weakened the migration, invasion and tumorigenesis ability of XWLC-05 cells. Sevoflurane may be a new treatment option for Xuanwei lung cancer.
- Sevoflurane /
- Xuanwei lung cancer /
- Apoptosis /
- Cell proliferation

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图 1 XWLC-05细胞克隆形成结果

与对照组相比，^**P < 0.01 。

Figure 1. XWLC-05 cell clone in two groups

下载: 全尺寸图片幻灯片

图 2 七氟烷处理后XWLC-05细胞凋亡结果

与对照组相比，^**P < 0.01。

Figure 2. Apoptosis of XWLC-05 cells after sevoflurane treatment

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图 3 XWLC-05细胞迁移和侵袭检测（×100）

Figure 3. XWLC-05 cell migration and invasion （×100）

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图 4 XWLC-05细胞迁移和侵袭检测统计

与对照组相比，^*P < 0.05，^**P < 0.01。

Figure 4. XWLC-05 cell migration and invasion detection statistics

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图 5 XWLC-05细胞成瘤后瘤体生长曲线

与对照组相比，^**P < 0.01。

Figure 5. Growth curve of XWLC-05 cells after tumorigenesis

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图 6 关键分子蛋白表达检测

Figure 6. Expression of key molecular proteins

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图 7 瘤体组织中关键分子蛋白表达检测统计

与对照组相比，^*P < 0.05，^**P < 0.01。

Figure 7. Detection and statistics of key molecular protein expression in tumor tissue

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