MiR-20a suppresses proliferation and facilitates apoptosis of breast cancer cells via the MTOR signaling pathway

Eur Rev Med Pharmacol Sci. 2020 Nov;24(22):11650-11657. doi: 10.26355/eurrev_202011_23809.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism
  • Apoptosis
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Cell Proliferation
  • Cells, Cultured
  • Female
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Signal Transduction
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Adaptor Proteins, Signal Transducing
  • LAMTOR3 protein, human
  • MIRN20a microRNA, human
  • MicroRNAs
  • MTOR protein, human
  • TOR Serine-Threonine Kinases