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In vivo and in vitro impact of miRNA-153 on the suppression of cell growth apoptosis through mTORC2 signaling pathway in breast cancer
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2021-08-29 , DOI: 10.1080/10799893.2021.1970766
Haimei Liu 1 , Hongyan Zang 2 , Jilin Kong 2 , Liguo Gong 2
Affiliation  

Abstract

Purpose

To investigate the effects and mechanism of miRNA-153 on breast cancer cells in vitro and in vivo.

Material and methods

The cells and mice were divided into five groups: miRNA-153 mimic, miRNA-153 NC, miRNA-153 inhibitor, miRNA-153 inhibitor-NC, and blank control groups. The real-time PCR and western blot were used to detect the rictor expression regulated by miRNA-153. The western blot was used to explore the expression levels of p-Akt Ser473, p-SGK1 Ser422, and p-FOXO1 Thr24 regulated by miRNA-153. The H&E stain was used to detect the morphology and vitality of tumor cells. Flow cytometry analysis or TUNEL detection was used to evaluate the apoptosis of tumor cells.

Results

MiRNA-153 was significantly reduced in breast cancer cell lines. The real-time PCR and western blot assay suggested that the miRNA-153 downregulation of rictor expression, which was correlated with the antitumor effects both in vitro and in vivo. The western blot assay also showed that the expression levels of p-Akt Ser473, p-SGK1 Ser422, and p-FOXO1 Thr24 were largely reduced in miRNA-153 treated group, which indicated that miRNA-153 inhibited breast cancer growth by regulation of mTORC2 signaling pathway. The H&E stain demonstrated that the morphology and vitality of tumor cells in tumor tissues were influenced in miRNA-153 mimic treated group. The TUNEL detection also showed a great quantity of apoptotic cells in the miRNA-153 mimic group.

Conclusions

All these results uncovering that the miRNA-153 inhibited breast cancer growth via regulation of mTORC2 signaling pathway, which provided breast cancer treatment a novel direction.



中文翻译:

miRNA-153通过mTORC2信号通路抑制乳腺癌细胞生长凋亡的体内外影响

摘要

目的

探讨miRNA-153在体外体内对乳腺癌细胞的作用及其机制。

材料与方法

将细胞和小鼠分为五组:miRNA-153模拟组、miRNA-153 NC组、miRNA-153抑制剂组、miRNA-153抑制剂-NC组和空白对照组。采用实时荧光定量 PCR 和蛋白质印迹法检测 miRNA-153 调控的 rictor 表达。采用western blot检测miRNA-153调控的p-Akt Ser473、p-SGK1 Ser422和p-FOXO1 Thr24的表达水平。H&E染色用于检测肿瘤细胞的形态和活力。流式细胞仪分析或TUNEL检测用于评估肿瘤细胞的凋亡。

结果

miRNA-153 在乳腺癌细胞系中显着减少。实时荧光定量 PCR 和蛋白质印迹分析表明 miRNA-153 下调 rictor 表达,这与体外体内的抗肿瘤作用相关。免疫印迹分析还显示,miRNA-153处理组p-Akt Ser473、p-SGK1 Ser422和p-FOXO1 Thr24的表达水平大幅降低,表明miRNA-153通过调节mTORC2抑制乳腺癌生长。信号通路。H&E染色表明,miRNA-153模拟物处理组肿瘤组织中肿瘤细胞的形态和活力受到影响。TUNEL检测还显示miRNA-153模拟组中有大量凋亡细胞。

结论

这些结果揭示了miRNA-153通过调节mTORC2信号通路抑制乳腺癌的生长,为乳腺癌的治疗提供了一个新的方向。

更新日期:2021-08-29
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