mTOR Activation by PI3K/Akt and ERK Signaling in Short ELF-EMF Exposed Human Keratinocytes

PLoS One. 2015 Oct 2;10(10):e0139644. doi: 10.1371/journal.pone.0139644. eCollection 2015.

Abstract

Several reports suggest that ELF-EMF exposures interact with biological processes including promotion of cell proliferation. However, the molecular mechanisms by which ELF-EMF controls cell growth are not completely understood. The present study aimed to investigate the effect of ELF-EMF on keratinocytes proliferation and molecular mechanisms involved. Effect of ELF-EMF (50 Hz, 1 mT) on HaCaT cell cycle and cells growth and viability was monitored by FACS analysis and BrdU assay. Gene expression profile by microarray and qRT-PCR validation was performed in HaCaT cells exposed or not to ELF-EMF. mTOR, Akt and MAPKs expressions were evaluated by Western blot analysis. In HaCaT cells, short ELF-EMF exposure modulates distinct patterns of gene expression involved in cell proliferation and in the cell cycle. mTOR activation resulted the main molecular target of ELF-EMF on HaCaT cells. Our data showed the increase of the canonical pathway of mTOR regulation (PI3K/Akt) and activation of ERK signaling pathways. Our results indicate that ELF-EMF selectively modulated the expression of multiple genes related to pivotal biological processes and functions that play a key role in physio-pathological mechanisms such as wound healing.

MeSH terms

  • Cell Culture Techniques
  • Cell Proliferation / genetics
  • Electromagnetic Fields
  • Humans
  • Keratinocytes / metabolism*
  • MAP Kinase Signaling System / genetics*
  • Male
  • Middle Aged
  • Multigene Family / genetics
  • Phosphatidylinositol 3-Kinases / genetics*
  • Proto-Oncogene Proteins c-akt / genetics*
  • Signal Transduction / genetics*
  • TOR Serine-Threonine Kinases / genetics*
  • Transcriptome / genetics
  • Wound Healing / genetics

Substances

  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases

Grants and funding

This work has been supported by Ministero dell’Università e della Ricerca (MIUR).