Literature DB >> 31966798

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

Junhong Cai1, Ying Zhang2, Sizhe Huang2, Mengdan Yan3, Jingjie Li3, Tianbo Jin3,4, Shan Bao2.   

Abstract

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.
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.
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. IJCEP
Copyright © 2017.

Entities:  

Keywords:  Beclin1; LC3B; autophagy; endometrial endometrioid adenocarcinoma (EEC); mTOR; microRNA (miRNA)

Year:  2017        PMID: 31966798      PMCID: PMC6965939     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


  6 in total

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  6 in total

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