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1.徐州市肿瘤医院肿瘤内科,江苏 徐州 221000
2.徐州市肿瘤医院普外科,江苏 徐州 221000
3.徐州市肿瘤医院检验科,江苏 徐州221000
赵鸿鹰,E-mail:a1i7dw@163.com
收稿:2025-02-25,
纸质出版:2026-01-25
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赵鸿鹰,江荣科,李艳芳等.miR-339-5p对胃癌细胞恶性生物学行为的影响机制研究[J].局解手术学杂志,2026,35(01):12-17.
ZHAO Hong-ying,JIANG Rong-ke,LI Yan-fang,et al.Mechanism of miR-339-5p in regulating malignant biological behavior of gastric cancer cells[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2026,35(01):12-17.
赵鸿鹰,江荣科,李艳芳等.miR-339-5p对胃癌细胞恶性生物学行为的影响机制研究[J].局解手术学杂志,2026,35(01):12-17. DOI: 10.11659/jjssx.02E025124.
ZHAO Hong-ying,JIANG Rong-ke,LI Yan-fang,et al.Mechanism of miR-339-5p in regulating malignant biological behavior of gastric cancer cells[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2026,35(01):12-17. DOI: 10.11659/jjssx.02E025124.
目的
2
探究miR-339-5p调控Akt/MDM2/p53信号通路对胃癌细胞恶性生物学行为的影响。
方法
2
收集2023年10月至2024年9月在我院手术切除的48例胃癌患者的癌组织及癌旁组织样本。利用qRT-PCR检测miR-339-5p在胃癌组织及细胞中的表达。将胃癌细胞NCI-N87分为control组(未进行转染)、miR-NC组(转染miR-339-5p mimics阴性对照质粒)、miR-339-5p mimics组(转染miR-339-5p mimics)、miR-339-5p mimics+SC-79组(转染miR-339-5p mimic后加入Akt激活剂SC-79)、miR-339-5p mimics+pcDNA组(共转染miR-339-5p mimics和空载质粒pcDNA)、miR-339-5p mimics+pc-MDM2组(共转染miR-339-5p mimics与MDM2过表达质粒pc-MDM2)。采用平板克隆形成实验和细胞划痕实验检测胃癌细胞增殖能力,Transwell实验检测胃癌细胞迁移和侵袭能力;通过双荧光素酶基因实验验证MDM2和miR-339-5p之间的靶向关系;Western blot检测Akt/MDM2/p53信号通路相关蛋白的表达水平。
结果
2
胃癌组织及细胞中miR-339-5p表达显著降低。与control组和miR-NC组比较,miR-339-5p mimics组细胞克隆形成数、划痕愈合率、细胞迁移数和侵袭数显著减少/下降,pAkt/Akt和pMDM2/MDM2水平降低,p53蛋白表达明显升高,差异均有统计学意义(
P
<
0.05)。激活Akt和过表达MDM2均可逆转miR-339-5p mimics对NCI-N87细胞上述指标的影响。双荧光素酶基因实验证实,miR-339-5p与MDM2存在靶向关系。
结论
2
miR-339-5p可能通过抑制Akt/MDM2/p53信号通路,影响胃癌细胞恶性生物学行为。
Objective
2
To investigate whether miR-339-5p affects the malignant biological behavior of gastric cancer cells through regulating Akt/MDM2/p53 signaling pathway.
Methods
2
The surgically removed cancer tissues and adjacent tissues were collected in our hospital from 48 gastric cancer patients from October 2023 to September 2024.The expression of miR-339-5p in tissues and cells of gastric cancer was detected by qRT-PCR.The gastric cancer cells NCI-N87 were divided into the control group (without transfection),miR-NC group (transfected with negative control plasmid of miR-339-5p mimics),miR-339-5p mimics group(transfected with miR-339-5p mimics),miR-339-5p mimics+SC-79 group (transfected with miR-339-5p mimics followed by the addition of Akt activator SC-79), miR-339-5p mimics+pcDNA group (co-transfected with miR-339-5p mimics and empty plasmid pcDNA), and miR-339-5p mimics+pc-MDM2 group (co-transfected with miR-339-5p mimics and MDM2 overexpression plasmid pc-MDM2). The proliferation ability of gastric cancer cells was detected by plate colony formation assay and scratch wound healing assay,and the migration and invasion abilities of gastric cancer cells were detected by Transwell assay.The targeting relationship between MDM2 and miR-339-5p was determined by dual luciferase reporter assay.The expression levels of proteins related to Akt/MDM2/p53 signaling pathway were detected by Western blot.
Results
2
miR-339-5p expression significantly decreased in gastric cancer tissues and cells. Compared with the control group and the miR-NC group, the number of colony cells, wound healing rate, and numbers of migration and invasion cells in the miR-339-5p mimics group were significantly reduced, the levels of pAkt/Akt and pMDM2/MDM2 decreased, and p53 protein expression significantly increased, with statistically significant differences (
P
<
0.05). Activation of Akt and overexpression of MDM2 could both reverse the effects of miR-339-5p mimics on the above indicators in NCI-N87 cells. Dual-luciferase reporter assays confirmed the targeting relationship between miR-339-5p and MDM2.
Conclusion
2
miR-339-5p suppresses the malignant biological behavior of gastric cancer cells via inhibiting the Akt/MDM2/p53 signaling pathway.
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