EYA1 通过调控PTEN/PI3K/AKT信号通路抑制胃癌SGC-7901 细胞的恶性生物学行为 |
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引用本文: | 朱红亚,罗子俨Δ,李平昴,刘佳佳.EYA1 通过调控PTEN/PI3K/AKT信号通路抑制胃癌SGC-7901 细胞的恶性生物学行为[J].中国肿瘤生物治疗杂志,2019,26(3):287-292. |
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作者姓名: | 朱红亚 罗子俨Δ 李平昴 刘佳佳 |
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作者单位: | 1.德阳市第二人民医院 普外科,四川 德阳 618000;2. 陆军军医大学附属西南医院全军普通外科中心,重庆400038 |
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基金项目: | 西部战区军事医学科技创新计划资助项目(No.SWH2016JCYB-48) |
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摘 要: | 摘要] 目的:探讨EYA1(eyes absent 1)通过调控PTEN/PI3K/AKT信号通路抑制胃癌SGC-7901细胞的恶性进展及其相关机制。方法:收集2016年6月至2018年6月陆军军医大学附属西南医院全军普通外科中心29例胃癌组织及其癌旁组织标本,采用Wb和qPCR实验检测胃癌组织和癌旁组织中EYA1 mRNA和蛋白的表达水平。人胃癌细胞株SGC-7901培养完成后,采用过表达EYA1质粒或siRNA干扰质粒转染胃癌SGC-7901细胞;分别采用MTT、流式细胞术、划痕愈合和Transwell实验检测胃癌SGC-7901细胞的增殖、凋亡、迁移和侵袭能力。结果:胃癌组织中EYA1 mRNA 和蛋白表达水平较癌旁组织均明显降低(P<0.01);过表达EYA1可明显提高SGC-7901 细胞的增殖、迁移和侵袭能力(均P<0.05)、抑制细胞凋亡(P<0.05)。过表达EYA1 可明显促进PTEN的表达、抑制PI3K/AKT通路的激活(均P<0.05或P<0.01);但在PTEN干扰后以上作用均受到了明显抑制(均P<0.05或P<0.01)。结论:EYA1可通过促进PTEN的表达抑制PI3K/AKT信号通路,从而抑制胃癌SGC-7901细胞的恶性生物学行为。
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关 键 词: | EYA1 PTEN/PI3K/AKT信号通路 胃癌 SGC-7901 细胞 增殖 凋亡 迁移 侵袭 |
收稿时间: | 2018/12/27 0:00:00 |
修稿时间: | 2019/2/12 0:00:00 |
EYA1 inhibits malignant biological behavior of gastric cancer SGC-7901 cells by regulating PTEN/PI3K/AKT signaling pathway |
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Affiliation: | 1. Department of General Surgery, the Second People''s Hospital of Deyang City, Deyang 618000, Sichuan, China; 2. General Surgery Center, Southwest Hospital Affiliated to Military Medical University,Chongqing 400038, China |
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Abstract: | Abstract] Objective:To explore the mechanism of EYA1 (eyes absent 1) inhibiting the malignant progression of gastric cancer SGC-7901 cells through regulating PTEN/PI3K/AKT signaling pathway. Methods: Twenty-nine pairs of gastric cancer tissues and para-cancerous tissues collected at the General Surgery center, Southwest Hospital Affiliated to Military Medical University during June 2016 and June 2018 were used in this study. Wb and RT-PCR assays were used to test the mRNA and protein expressions of EYA1 in gastric cancer tissues and the paired para-cancerous tissues; Transfection with plasmid or siRNAs were used to up-regulate or down-regulate EYA1 or PTEN expression in gastric cancer SGC-7901 cells; MTT, Flow Cytometry, Wound Healing and Transwell assays were carried out to detect cell proliferation, apoptosis, metastasis and invasion abilities, respectively. Results: EYA1 expression was decreased in gastric cancer tissues as compared with the para-cancerous tissues at both mRNA and protein levels (P<0.01); EYA1 over-expression significantly enhanced the proliferation, metastasis and invasion of SGC-7901 cells (all P<0.05), and inhibited cell apoptosis (P<0.05);moreover, its over-expressionsignificantly increased the expression of PTEN, and inhibited the activation of PI3K/AKT pathway (all P<0.05 or P<0.01). However, the above effects mediated by EYA1 up-regulation were significantly impaired after the knockout of PTEN (all P<0.05 or P<0.01). Conclusion: EYA1 can inhibit the malignant progression of gastric cancer SGC-7901 cells through promoting the expression of PTEN and activating PI3K/AKT pathway. |
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