MiR-100-5p, miR-199a-3p and miR-199b-5p induce autophagic death of endometrial carcinoma cell through targeting mTOR

miR-100-5p、miR-199a-3p和miR-199b-5p通过靶向mTOR诱导子宫内膜癌细胞自噬死亡

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作者:Junhong Cai, Ying Zhang, Sizhe Huang, Mengdan Yan, Jingjie Li, Tianbo Jin, Shan Bao

Conclusions

Our results suggested that miR-100-5p, miR-199a-3p and miR-199b-5p may induce the autophagic death of EEC cell through targeting mTOR.

Methods

The effects of three miRNAs on proliferation and apoptosis in EEC cells were analyzed in KLE and ISK cells transfected with miR-100-5p, miR-199a-3p and miR-199b-5p mimics and inhibitors. Quantitative real-time polymerase chain reaction (qRT-PCR), CCK-8 method, flow cytometry and luciferase reporter assay were used to assess the effects of three miRNAs on cell viability, proliferation, apoptosis, and autophagy.

Objective

The study aimed to explore the association between three miRNAs (miR-100-5p, miR-199a-3p and miR-199b-5p) and mTOR induced autophagy in EEC cells. The expression of three miRNAs and autophagy-related genes Beclin1 and LC3 in Ishikawa and KLE cells were detected.

Results

We found an increased expression of Beclin1 and LC3 in Ishikawa and KLE cells transfected by miR-100-5p, miR-199a-3p and miR-199b-5p mimics compared with NC (P<0.05). Additionally, Ishikawa and KLE cells transfected with miR-100-5p, miR-199a-3p and miR-199b-5p mimics grew more slowly than mock and mimics control (P<0.05); we also found an increased apoptosis incidence of Ishikawa cell transfected with miR-100-5p, miR-199a-3p and miR-199b-5p mimics (P<0.05). Finally, luciferase reporter results showed miR-100-5p, miR-199a-3p and miR-199b-5p were all down-regulated the luciferase activity in cells transfected with miRNA mimics compared with mock. All results suggested that miR-100-5p, miR-199a-3p and miR-199b-5p may induce the autophagic death of EEC cell through targeting mTOR. Conclusions: Our results suggested that miR-100-5p, miR-199a-3p and miR-199b-5p may induce the autophagic death of EEC cell through targeting mTOR.

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