首页|基于miR-34a/HMGB1轴探讨七氟醚对胃癌细胞恶性生物学活性的机制

基于miR-34a/HMGB1轴探讨七氟醚对胃癌细胞恶性生物学活性的机制

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目的 基于miR-34a/HMGB1轴探究七氟醚对胃癌细胞恶性生物学活性的影响.方法 将胃癌细胞分为 NC 组,SEV-1.7%组、SEV-3.4%组、SEV-5.1%组.miR-34a 组、SEV-5.1%+anti-miR-34a 组、SEV-5.1%+pcDNA-HMGB1 组和SEV-5.1%+pcDNA-HMGB 1+miR-34a组.CCK-8、Transwell小室法分别检测细胞增殖和侵袭移能力;qRT-PCR检测miR-34a表达;蛋白质印迹检测细胞中HMGB1蛋白表达;双荧光素酶报告系统实验检测miR-34a和HMGB1的靶向关系.结果 和GES-1细胞系相比,胃癌SGC-7901细胞(0.23± 0.03)中 miR-34a 表达降低,HMGB1 蛋白(0.85±0.10)表达升高(P<0.05).和 NC 组相比,SEV-1.7%组、SEV-3.4%组、SEV-5.1%组细胞中miR-34a表达均升高,细胞存活率、细胞侵袭数目和HMGB1蛋白表达均降低(P<0.05).和 SEV-5.1%组相比,SEV-5.1%+anti-miR-34a组细胞存活率[24 h、48 h 分别为(92.46±8.27)%、(96.71±7.52)%]、细胞侵袭数目(126.42±10.84)和细胞中HMGB 1蛋白(0.80±0.09)表达均明显增加(P<0.05).向细胞中转染HMGB 1-WT时,miR-34a组(0.34±0.05)荧光素酶活性明显低于miR-NC组(P<0.05).和 SEV-5.1%组相比,SEV-5.1%+pcDNA-HMGB1 组细胞存活率[24 h、48 h 分别为(90.18±8.06)%、(82.47± 7.21)%]、细胞侵袭数目(122.18±10.62)和细胞中HMGB1蛋白(0.81±0.10)表达均明显升高(P<0.05);和SEV-5.1%+pcDNA-HMGB1 组相比,SEV-5.1%+pcDNA-HMGB 1+miR-34a组细胞存活率[24 h、48 h 分别为(65.33± 6.02)%、(28.41±3.26)%]、细胞侵袭数目(68.33±6.09)和细胞中HMGB 1蛋白(0.34±0.04)表达均明显降低(P<0.05).结论 七氟醚可通过调节miR-34a/HMGB1轴抑制胃癌细胞增殖和侵袭.
Exploration of the mechanism of sevoflurane on malignant biological activity of gastric cancer cells based on miR-34a/HMGB1 axis
Objective To explore the effect of sevoflurane on the malignant biological activity of gastric can-cer cells based on the miR-34a/HMGB1 axis.Methods The gastric cancer cells were divided into groups including the NC group,SEV-1.7%group,SEV-3.4%group,and SEV-5.1%group.Additionally,there were groups including the miR-34a group,SEV-5.1%+anti-miR-34a group,SEV-5.1%+pcDNA-HMGB1 group,and SEV-5.1%+pcDNA-HMGB1+miR-34a group.Cell proliferation was assessed using the CCK-8 assay,while cell invasion and migration capabilities were assessed using the Transwell chamber assay.The expression of miR-34a was measured using qRT-PCR,and the expression of HMGB1 protein in cells was detected using Western blot analysis.The targeting relation-ship between miR-34a and HMGB1 was investigated using a dual luciferase reporter system experiment.Results Compared to the GES-1 cell line,miR-34a expression was downregulated(0.23±0.03)and HMGB1 protein expres-sion was upregulated(0.85±0.10)in gastric cancer SGC-7901 cells(P<0.05).Compared to the NC group,miR-34a expression increased and cell viability,cell invasion,and HMGB1 protein expression decreased in the SEV-1.7%group,SEV-3.4%group,and SEV-5.1%group(P<0.05).Compared to the SEV-5.1%group,cell viability(92.46%±8.27%,96.71%±7.52%in 24 h and 48 h,respectively),cell invasion(126.42±10.84),and HMGB1 protein expression(0.80±0.09)significantly increased in the SEV-5.1%+anti-miR-34a group(P<0.05).When trans-fecting HMGB1-WT into cells,the luciferase activity of the miR-34a group(0.34±0.05)was significantly lower than that of the miR-NC group(P<0.05).Compared to the SEV-5.1%group,cell viability(90.18%±8.06%,82.47%± 7.21%in 24 h and 48 h,respectively),cell invasion(122.18±10.62),and HMGB1 protein expression(0.81± 0.10)significantly increased in the SEV-5.1%+pcDNA-HMGB1 group(P<0.05).Compared to the SEV-5.1%+pcD-NA-HMGB1 group,cell viability(65.33%±6.02%,28.41%±3.26%in 24 h and 48 h,respectively),cell invasion(68.33±6.09),and HMGB1 protein expression(0.34±0.04)significantly decreased in the SEV-5.1%+pcDNA-HMGB1+miR-34a group(P<0.05).Conclusion Sevoflurane can inhibit the proliferation and invasion of gastric cancer cells by regulating the miR-34a/HMGB1 axis.

Gastric cancer cellsSevofluraneMiR-34a/HMGB1 axisProliferationInvasion

胥晓倩、欧阳欣、周李平、陈祖棋、王红霞、邬龄

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成都医学院附属第二医院·核工业四一六医院,四川成都 610051

胃癌细胞 七氟醚 miR-34a/HMGB1轴 增殖 侵袭

成都市医学科研课题

2020109

2024

解剖学研究
广东省解剖学会 中国解剖学会

解剖学研究

CSTPCD
影响因子:0.327
ISSN:1671-0770
年,卷(期):2024.46(1)
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