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唐山市人民医院消化科,河北 唐山 063000
马丽丽,E-mail:mll061@126.com
收稿日期:2024-05-22,
纸质出版日期:2025-07-25
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杜艳明,崔丽伟,檀靖宇等.雷公藤甲素对胃癌细胞增殖、迁移及侵袭的影响及机制研究[J].局解手术学杂志,2025,34(07):595-599.
DU Yan-ming,CUI Li-wei,TAN Jing-yu,et al.Effect of triptolide on proliferation, migration and invasion of gastric cancer cells and its mechanism[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(07):595-599.
杜艳明,崔丽伟,檀靖宇等.雷公藤甲素对胃癌细胞增殖、迁移及侵袭的影响及机制研究[J].局解手术学杂志,2025,34(07):595-599. DOI: 10.11659/jjssx.05E024103.
DU Yan-ming,CUI Li-wei,TAN Jing-yu,et al.Effect of triptolide on proliferation, migration and invasion of gastric cancer cells and its mechanism[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(07):595-599. DOI: 10.11659/jjssx.05E024103.
目的
2
探讨雷公藤甲素(TPL)对胃癌细胞增殖、迁移、侵袭的影响及其作用机制。
方法
2
体外培养人胃癌细胞系MKN45,给予不同浓度的TPL作用48 h,CCK-8法检测细胞增殖抑制率并选取最佳浓度进行后续实验,qRT-PCR检测经不同浓度TPL处理后的细胞miR-29b、KDM2A mRNA表达。取对数生长期MKN45细胞,随机分为对照组(不做任何处理)、TPL组(200 μg/mL TPL处理)、inhibitor-NC+TPL组(转染inhibitor-NC后用200 μg/mL TPL处理)、miR-29b inhibitor+TPL组(转染miR-29b inhibitor后用200 μg/mL TPL处理),qRT-PCR检测各组细胞miR-29b、KDM2A mRNA表达,Western blot检测各组细胞KDM2A蛋白表达,平板克隆形成实验检测各组细胞克隆形成能力,Transwell实验检测各组细胞迁移、侵袭能力。
结果
2
25 μg/mL、50 μg/mL、100 μg/mL、200 μg/mL浓度的TPL均可明显抑制MKN45细胞增殖(
P
<
0.05),上调细胞中miR-29b表达(
P
<
0.05),下调KDM2A mRNA表达(
P
<
0.05),且TPL浓度为200 μg/mL时作用最明显,故选择200 μg/mL的TPL进行后续实验。与对照组比较,TPL组细胞miR-29b表达升高(
P
<
0.05),KDM2A mRNA和蛋白表达降低(
P
<
0.05),克隆形成数、迁移及侵袭细胞数减少(
P
<
0.05)。与inhibitor-NC+TPL组比较,miR-29b inhibitor+TPL组细胞miR-29b表达降低(
P
<
0.05),KDM2A mRNA和蛋白表达升高(
P
<
0.05),克隆形成数、迁移及侵袭细胞数增加(
P
<
0.05)。
结论
2
TPL能抑制胃癌细胞增殖、迁移及侵袭,其机制与调控miR-29b/KDM2A信号通路有关。
Objective
2
To explore the effects of triptolide (TPL) on the proliferation,migration and invasion of gastric cancer cells and its mechanism.
Methods
2
Human gastric cancer cell line MKN45 was cultured in vitro and treated with different concentrations of TPL for 48 hours.The cell proliferation inhibition rate was detected by CCK-8 method and the optimal concentration was selected for subsequent experiments.qRT-PCR was used to detect the expression of miR-29b and KDM2A mRNA in cells treated with different concentrations of TPL.MKN45 cells at logarithmic growth phase were randomly divided into the control group (without any treatment),the TPL group (treated with 200 μg/mL TPL),the inhibitor-NC+TPL group (transfected with inhibitor-NC and then treated with 200 μg/mL TPL),and the miR-29b inhibitor+TPL group (transfected with miR-29b inhibitor and then treated with 200 μg/mL TPL).qRT-PCR was used to detect the expression of miR-29b and KDM2A mRNA in each group of cells,and Western blot was used to detect the expression of KDM2A protein.The clone formation ability of each group of cells was detected by plate clone formation assay,and the migration and invasion abilities of each group of cells were detected by Transwell assay.
Results
2
TPL at concentrations of 25 μg/mL,50 μg/mL,100 μg/mL,and 200 μg/mL could significantly inhibit the proliferation of MKN45 cells (
P
<
0.05),up-regulate the expression of miR-29b in cells (
P
<
0.05),and down-regulate the expression of KDM2A mRNA (
P
<
0.05).The effect was most obvious at the concentration of 200 μg/mL,so 200 μg/mL TPL was selected for the subsequent experiments.Compared with the control group,the expression of miR-29b in the TPL group increased (
P
<
0.05),the expression of KDM2A mRNA and protein decreased (
P
<
0.05),and the numbers of clone formation,migration and invasion cells reduced (
P
<
0.05).Compared with the inhibitor-NC+TPL group,the expression of miR-29b in the miR-29b inhibitor+TPL group decreased (
P
<
0.05),the expression of KDM2A mRNA and protein increased (
P
<
0.05),and the numbers o
f clone formation,migration and invasion cells increased (
P
<
0.05).
Conclusion
2
TPL can inhibit the proliferation,migration and invasion of gastric cancer cells,and its mechanism is related to the regulation of the miR-29b/KDM2A signaling pathway.
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