MiR-16-5p inhibits breast cancer by reducing AKT3 to restrain NF-κB pathway

Biosci Rep. 2019 Aug 23;39(8):BSR20191611. doi: 10.1042/BSR20191611. Print 2019 Aug 30.

Abstract

Background: Breast cancer endangers the life of women and has become the major cause of deaths among them. MiRNAs are found to exert a regulatory effect on the migration, proliferation and apoptosis of breast cancer cells. This research aims at investigating the miR-16-5p expression and its effect on the pathogenesis of breast cancer. Methods: Their clinical data were analyzed with qRT-PCR. CCK8, EdU and Transwell was performed to explore the function of miR-16-5p in cell migration and proliferation of breast cancer cells. Dual-luciferase reporter assay, immunohistochemistry and Western blotting were carried out to explore the relation between miR-16-5p and AKT3. Results: It was discovered that miR-16-5p was lowly expressed in breast cancer patients. Meanwhile, breast cancer patients with under-expressed miR-16-5p had a lower survival rate than those with highly expressed miR-16-5p. Furthermore, decreased miR-16-5p in cell and animal models enhanced migration and proliferation of breast cancer cells, stimulated cell cycle and reduced cell apoptosis. Finally, we found miR-16-5p restrained the NF-κB pathway and decreased AKT3 gene, thereby suppressing the breast cancer development. Conclusion: It can be seen that miR-16-5p exhibits a low expression in breast cancer tissues, which can inhibit breast cancer by restraining the NF-κB pathway and elevating reducing AKT3.

Keywords: AKT3; NF-κB; breast cancer; metastasis; miRNA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Retracted Publication

MeSH terms

  • Animals
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Female
  • Humans
  • MCF-7 Cells
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism*
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / metabolism*
  • Signal Transduction*

Substances

  • MIRN16 microRNA, human
  • MicroRNAs
  • NF-kappa B
  • RNA, Neoplasm
  • AKT3 protein, human
  • Proto-Oncogene Proteins c-akt