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miR-183 通过靶向抑制 mTOR 增强 GC 细胞的自噬。

miR-183 Enhances Autophagy of GC Cells by Targeted Inhibition of mTOR.

机构信息

Department of Medical Oncology, Hebei Key Laboratory of Cancer Radiotherapy and Chemotherapy, Baoding, Hebei, China.

Department of Pathology, Affiliated Hospital of Hebei University, Baoding, Hebei, China.

出版信息

Ann Clin Lab Sci. 2021 Nov;51(6):837-843.

Abstract

OBJECTIVE

We investigated whether miR-183 played a role in regulating mTOR expression and influencing autophagy of GC cells.

METHODS

Tumor tissues and paracancerous tissues were collected from GC patients to detect the expressions of miR-183, mTOR, autophagy-related proteins Beclin-1. SGC-7901 cells were cultured and divided into 5 groups: MiR-NC group, MiR-183 mimic group, si-NC group, small interfering RNA transfected (si)-mTOR group, miR-183 mimic + si-mTOR group, to compare the expression of mTOR, apoptosis rate and clonality in all groups, and detect the expressions of Beclin-1 under starvation condition.

RESULTS

The expressions of miR-183, Beclin-1 in GC tissues were significantly decreased, and the expression of mTOR was significantly increased compared with those in paracancerous tissues. There was a targeted-regulating relationship between miR-183 and mTOR. Compared with GES-1 cells, miR-183 expression was decreased and mTOR expression was increased in SGC-7901 cells, and under starvation condition, the expressions of Beclin-1 were decreased. After transfected with miR-183 mimic and/or si-mTOR, the expression of mTOR in SGC-7901 cells was decreased significantly, the cell clonality was significantly reduced, apoptosis was increased significantly, and cell autophagy activity induced by starvation was significantly enhanced.

CONCLUSION

miR-183 can influence the proliferation, apoptosis and autophagy of GC cells through targeted inhibition of mTOR expression.

摘要

目的

研究 miR-183 是否在调节 mTOR 表达和影响 GC 细胞自噬中发挥作用。

方法

收集 GC 患者的肿瘤组织和癌旁组织,检测 miR-183、mTOR、自噬相关蛋白 Beclin-1 的表达。培养 SGC-7901 细胞,分为 5 组:miR-NC 组、miR-183 模拟组、si-NC 组、转染小干扰 RNA(si)-mTOR 组、miR-183 模拟+si-mTOR 组,比较各组 mTOR 表达、细胞凋亡率和克隆形成率,并在饥饿条件下检测 Beclin-1 的表达。

结果

GC 组织中 miR-183、Beclin-1 的表达明显降低,mTOR 的表达明显升高,与癌旁组织相比。miR-183 与 mTOR 之间存在靶向调控关系。与 GES-1 细胞相比,SGC-7901 细胞中 miR-183 的表达降低,mTOR 的表达升高,在饥饿条件下,Beclin-1 的表达降低。转染 miR-183 模拟物和/或 si-mTOR 后,SGC-7901 细胞中 mTOR 的表达明显降低,细胞克隆形成率明显降低,细胞凋亡明显增加,饥饿诱导的细胞自噬活性明显增强。

结论

miR-183 可通过靶向抑制 mTOR 表达影响 GC 细胞的增殖、凋亡和自噬。

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