| 张婧博,高瑞君,王力彬,杨柳.lncRNA-LAMTOR5-AS1通过缺氧胃癌细胞外泌体靶向miR-331-3p调控胃癌BGC-823细胞恶性行为.[J].中南医学科学杂志.,2025,(6):957-962. |
| lncRNA-LAMTOR5-AS1通过缺氧胃癌细胞外泌体靶向miR-331-3p调控胃癌BGC-823细胞恶性行为 |
| lncRNA-LAMTOR5-AS1 regulates malignant behavior of gastric cancer BGC-823 cells by targeting miR-331-3p in exosomes of hypoxic gastric cancer cells |
| 投稿时间：2025-04-17 修订日期：2025-08-12 |
| DOI：10.15972/j.cnki.43-1509/r.2025.06.004 |
| 中文关键词: 外泌体 LAMTOR5-AS1 miR-331-3p 胃癌 BGC-823 缺氧 |
| 英文关键词:exosomes LAMTOR5-AS1 miR-331-3p gastric cancer BGC-823 hypoxia |
| 基金项目:咸阳市重点研发计划项目(L2022ZDYFSF062)；陕西能源职业技术学院青年教师专项项目(2021QN03) |
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| 中文摘要: |
| 目的探讨lncRNA-LAMTOR5-AS1通过缺氧胃癌细胞外泌体靶向miR-331-3p对胃癌BGC-823细胞的影响。 方法于常氧和缺氧条件下培养胃癌BGC-823细胞,收集对应外泌体为N-exo和H-exo；于缺氧条件下转染短发夹(sh)-LAMTOR5-AS1及其阴性对照sh-NC,收集对应外泌体为sh-LAMTOR5-AS1-H-exo和sh-NC-H-exo。透射电镜和蛋白质印迹法鉴定外泌体。将BGC-823细胞分为CK组(PBS培养)、N-EXO组(N-exo培养)、H-EXO组(H-exo培养)、sh-NC-H-EXO组(sh-NC-H-exo培养)、sh-LAMTOR5-AS1-H-EXO组(sh-LAMTOR5-AS1-H-exo培养)、sh-LAMTOR5-AS1-H-EXO+inhibitor NC组(sh-LAMTOR5-AS1-H-exo+inhibitor NC培养)和sh-LAMTOR5-AS1-H-EXO+miR-331-3p inhibitor组(sh-LAMTOR5-AS1-H-exo+miR-331-3p inhibitor培养)。采用qRT-PCR检测细胞LAMTOR5-AS1、miR-331-3p表达水平。采用CCK-8法、Transwell实验、流式细胞术分别检测各组细胞增殖、迁移和侵袭能力、细胞凋亡率。Western blotting检测各组细胞相关蛋白表达水平。 结果N-exo和H-exo均可促进BGC-823细胞恶性生物学行为(P＜0.05)；H-exo对BGC-823细胞的促进作用优于N-exo(P＜0.05)；敲除LAMTOR5-AS1可降低H-exo对BGC-823细胞的恶性生物学行为的促进作用(P＜0.05)；下调miR-331-3p表达可部分逆转敲除LAMTOR5-AS1的作用(P＜0.05)。 结论缺氧诱导胃癌细胞外泌体LAMTOR5-AS1可促进胃癌细胞恶性生物学行为,其机制可能与调控miR-331-3p表达,激活磷脂酰肌醇3激酶/蛋白激酶B信号通路有关。 |
| 英文摘要: |
| AimTo explore the effect of lncRNA-LAMTOR5-AS1 on gastric cancer BGC-823 by targeting miR-331-3p in exosomes of hypoxic gastric cancer cells. MethodsGastric cancer BGC-823 cells were cultivated under normoxic and hypoxic conditions, and corresponding exosomes N-exo and H-exo were collected; The short hairpin (sh)-LAMTOR5-AS1 were transfected with its negative control sh-NC under hypoxic conditions, and the corresponding sh-LAMTOR5-AS1-H-exo and sh-NC-H-exo were collected.Exosomes were identified using transmission electron microscopy and Western blotting. BGC-823 cells were divided into CK group (PBS culture), N-EXO group (N-exo culture), H-EXO group (H-exo culture), sh-NC-H-EXO group (sh-NC-H-exo culture), sh-LAMTOR5-AS1-H-EXO group (sh-LAMTOR5-AS1-H-exo culture), sh-LAMTOR5-AS1-H-EXO+inhibitor NC group (sh-LAMTOR5-AS1-H-exo+inhibitor NC culture), and sh-LAMTOR5-AS1-H-EXO+miR-331-3p inhibitor group (sh-LAMTOR5-AS1-H-exo+miR-331-3p inhibitor culture). qRT-PCR was used to detect the expression levels of LAMTOR5-AS1 and miR-331-3p in cells. The CCK-8 method, Transwell assay, and flow cytometry were used to detect the proliferation, migration and invasion ability, as well as apoptosis rate of each group of cells. Western blotting was used to detect the expression levels of cell related proteins in each group. ResultsBoth N-exo and H-exo promoted the malignant biological behavior of BGC-823 cells (P＜0.05); The promoting effect of H-exo on BGC-823 cells was superior to that of N-exo (P＜0.05); Knocking out LAMTOR5-AS1 reduced the promoting effect of H-exo on the malignant biological behavior of BGC-823 cells (P＜0.05); Downregulation of miR-331-3p expression partially reversed the knockout effect of LAMTOR5-AS1 (P＜0.05). ConclusionHypoxia induced extracellular vesicle LAMTOR5-AS1 in gastric cancer cells can promote malignant biological behavior, and its mechanism may be related to the regulation of miR-331-3p expression and activation of phosphoinositide 3-kinase/protein kinase B signaling pathway. |
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