PMID- 33275232 OWN - NLM STAT- MEDLINE DCOM- 20210629 LR - 20211204 IS - 2284-0729 (Electronic) IS - 1128-3602 (Linking) VI - 24 IP - 22 DP - 2020 Nov TI - MiR-20a suppresses proliferation and facilitates apoptosis of breast cancer cells via the MTOR signaling pathway. PG - 11650-11657 LID - 23809 [pii] LID - 10.26355/eurrev_202011_23809 [doi] AB - OBJECTIVE: The paper aimed to explore the role of micro ribonucleic acid (miR)-20a in regulating the proliferation and apoptosis of breast cancer cells. MATERIALS AND METHODS: The expression of miR-20a in breast cancer cells was analyzed via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. Cell Counting Kit-8 (CCK-8) assay, colony formation assay, and flow cytometry were employed to analyze the proliferation and apoptosis of cells. Thereafter, the target proteins of miR-20a were predicted using TargetScan, a website for miRNA target gene prediction, and the interaction between miR-20a and the target genes was detected through the Luciferase reporter gene assay, qRT-PCR assay, and Western blotting. Finally, the miR-20a inhibitor and target gene expression plasmids were co-transfected for rescue experiment to study whether the target genes participate in the inhibitory effect of miR-20a on the proliferation of breast cancer cells. RESULTS: It was found that the expression of miR-20a was upregulated in breast cancer cell lines. Silencing miR-20a expression inhibited the proliferation and promoted the apoptosis of breast cancer cell. Besides, it was demonstrated that late endosomal/lysosomal adaptor, mitogen-activated protein kinase (MAPK), and mammalian target of rapamycin (mTOR) activator 3 (LAMTOR3) were a direct target of miR-20a. The knockdown of LAMTOR3 expression repressed the influence of miR-20a on the proliferation of breast cancer cells. CONCLUSIONS: MiR-20a targets LAMTOR3 gene to regulate the mTOR signaling pathway, thereby suppressing the proliferation and facilitating the apoptosis of breast cancer cells. It suggests that miR-20a exerts a carcinogenic effect in breast cancer, which may be a potential target for the treatment of breast cancer. FAU - Shi, K-Y AU - Shi KY AD - Department of Ultrasound, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Zhejiang, China. wanglj@zjcc.org.cn. FAU - Fan, L-Y AU - Fan LY FAU - Xu, D AU - Xu D FAU - Ren, L-P AU - Ren LP FAU - Wang, L-P AU - Wang LP FAU - Chen, L-Y AU - Chen LY FAU - Wang, L-J AU - Wang LJ LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Italy TA - Eur Rev Med Pharmacol Sci JT - European review for medical and pharmacological sciences JID - 9717360 RN - 0 (Adaptor Proteins, Signal Transducing) RN - 0 (LAMTOR3 protein, human) RN - 0 (MIRN20a microRNA, human) RN - 0 (MicroRNAs) RN - EC 2.7.1.1 (MTOR protein, human) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) SB - IM MH - Adaptor Proteins, Signal Transducing/genetics/metabolism MH - Apoptosis MH - Breast Neoplasms/*metabolism/pathology MH - Cell Proliferation MH - Cells, Cultured MH - Female MH - Humans MH - MicroRNAs/genetics/*metabolism MH - Signal Transduction MH - TOR Serine-Threonine Kinases/genetics/*metabolism EDAT- 2020/12/05 06:00 MHDA- 2021/06/30 06:00 CRDT- 2020/12/04 12:08 PHST- 2020/12/04 12:08 [entrez] PHST- 2020/12/05 06:00 [pubmed] PHST- 2021/06/30 06:00 [medline] AID - 23809 [pii] AID - 10.26355/eurrev_202011_23809 [doi] PST - ppublish SO - Eur Rev Med Pharmacol Sci. 2020 Nov;24(22):11650-11657. doi: 10.26355/eurrev_202011_23809.