FGF represses metastasis of neuroblastoma regulated by MYCN and TGF-β1 induced LMO1 via control of let-7 expression

Brain Res. 2019 Feb 1:1704:219-228. doi: 10.1016/j.brainres.2018.10.015. Epub 2018 Oct 12.

Abstract

Background: MYCN and LMO1 amplification are commonly observed in neuroblastoma (NB), which was often accompanied by genetic loss of let-7 microRNA (miRNA). Fibroblast growth factor (FGF) was found to regulate let-7 miRNA expression via FGF receptor substrate 2 (FRS2), which then activates transforming growth factor beta (TGF-β) signaling.

Methods: Expression of MYCN, LMO1, FRS2, let-7, and TGF-β receptor I (TGFβRI) was selectively knocked-down or enhanced in NB cells. Proliferation, invasion, migration, metastasis and tumorigenesis of NB, expression of downstream signaling factors and metastasis-associated protein were evaluated.

Results: Knock-down on either MYCN or LMO1 has led to inhibition on proliferation, invasion, migration, and metastasis of NB cells, and knock-down of FRS2 resulted in increases in MYCN and LMO1 expression and enhanced invasion, migration and metastasis of NB cells. Decreased expression of TGF-β1 or TGFβRI led to decrease expression in LMO1 and proliferation, invasion, migration and metastasis markers, except MYCN expression which appeared not to be regulated by TGF-β1 or TGFβRI. Furthermore, let-7 miRNA was shown to decrease the expression levels of TGF-βRI, LMO1 and MYCN.

Conclusions: FGF regulates MYCN and TGF-β1-induced LMO1 and metastasis of NB cells via let-7 miRNA.

Keywords: FRS2; LMO1; MYCN; Neuroblastoma; TGFβRI; let-7 miRNA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Cell Line, Tumor
  • Cell Movement / physiology
  • Cell Proliferation / physiology
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Gene Knockdown Techniques
  • Humans
  • LIM Domain Proteins / genetics
  • LIM Domain Proteins / metabolism*
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • N-Myc Proto-Oncogene Protein / metabolism*
  • Neuroblastoma / metabolism*
  • Neuroblastoma / pathology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Neurons / pathology
  • Receptor, Transforming Growth Factor-beta Type I / genetics
  • Receptor, Transforming Growth Factor-beta Type I / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transforming Growth Factor beta1 / pharmacology

Substances

  • Adaptor Proteins, Signal Transducing
  • DNA-Binding Proteins
  • FRS2 protein, human
  • LIM Domain Proteins
  • Membrane Proteins
  • MicroRNAs
  • N-Myc Proto-Oncogene Protein
  • Transcription Factors
  • Transforming Growth Factor beta1
  • mirnlet7 microRNA, human
  • Receptor, Transforming Growth Factor-beta Type I