Neferine inhibits MDA-MB-231 cells growth and metastasis by regulating miR-374a/FGFR-2

Chem Biol Interact. 2019 Aug 25:309:108716. doi: 10.1016/j.cbi.2019.06.029. Epub 2019 Jun 15.

Abstract

Background: Neferine (NEF) is a major bisbenzylisoquinline alkaloid mainly exists in the seed embryo of Nelumbo nucifera (Gaertn.) that possesses anti-tumor effects. Our study designed to check the effect of NEF on breast cancer MDA-MB-231 cells and further explore the potential mechanism.

Methods: MDA-MB-231 cells were administrated with various dosages of NEF for 24 h after which cell viability was measured. The effects of NEF on cell proliferation, apoptosis, migration and invasion were assessed by BrdU staining, flow cytometry assay and Transwell assay. Western blot was utilized to assess the accumulation of proteins related with proliferation, apoptosis, metastasis, PI3K/AKT and MEK/ERK pathways.

Results: Viability was efficiently reduced by NEF in a dose-dependent manner. NEF (8 μM) significantly suppressed cell proliferation, migration and invasion but enhanced apoptosis in MDA-MB-213 cells. Interestingly, NEF suppressed miR-374a expression and miR-374a mediated the inhibitory effect of NEF. Moreover, miR-374a positively regulated FGFR-2 expression and FGFR-2 overexpression impeded the effect of NEF on MDA-MB-213 cells. FGFR-2 overexpression abolished the suppressive effect of NEF on PI3K/AKT and MEK/ERK pathways.

Conclusion: We found that NEF possessed the anti-growth and anti-metastasis effect on MDA-MB-231 cells through regulating miR-374a/FGFR-2, which might provide new insight for breast cancer management.

Keywords: Breast cancer; FGFR-2; Neferine; PI3K/AKT and MEK/ERK pathways; miR-374a.

MeSH terms

  • Antagomirs / metabolism
  • Benzylisoquinolines / pharmacology*
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects*
  • Down-Regulation / drug effects
  • Female
  • Humans
  • Matrix Metalloproteinase 2 / genetics
  • Matrix Metalloproteinase 2 / metabolism
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA Interference
  • RNA, Small Interfering / metabolism
  • Receptor, Fibroblast Growth Factor, Type 2 / antagonists & inhibitors
  • Receptor, Fibroblast Growth Factor, Type 2 / genetics
  • Receptor, Fibroblast Growth Factor, Type 2 / metabolism*
  • Signal Transduction / drug effects

Substances

  • Antagomirs
  • Benzylisoquinolines
  • MIRN374 microRNA 374, human
  • MicroRNAs
  • RNA, Small Interfering
  • neferine
  • Phosphatidylinositol 3-Kinases
  • FGFR2 protein, human
  • Receptor, Fibroblast Growth Factor, Type 2
  • Proto-Oncogene Proteins c-akt
  • Matrix Metalloproteinase 2