Cross-talk between non-ionizing electromagnetic fields and metastasis; EMT and hybrid E/M may explain the anticancer

Romina Mehdizadeh1, Alireza Madjid Ansari2, Flora Forouzesh1

  • 1Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.

Insights

Non-ionizing electromagnetic fields (NIEMFs) show anti-cancer potential by influencing metastasis. This study explores how NIEMFs affect epithelial-mesenchymal transition (EMT) pathways, crucial for cancer spread.

Area of Science:

  • Biophysics
  • Oncology
  • Cell Biology

Background:

  • Non-ionizing electromagnetic fields (NIEMFs) exhibit potential anti-cancer properties against various cancer cells.
  • Metastasis, the spread of cancer, is a primary cause of cancer-related mortality and involves complex cellular processes.
  • Epithelial-mesenchymal transition (EMT) is a key biological process implicated in cancer metastasis, embryogenesis, and tissue regeneration.

Purpose of the Study:

  • To elucidate the precise mechanisms by which NIEMFs exert anti-cancer effects.
  • To investigate the potential impact of NIEMFs on critical epithelial-mesenchymal transition (EMT) molecules and pathways involved in cancer metastasis.

Main Methods:

  • Literature review and critical analysis of existing studies on NIEMFs and cancer.
  • Discussion of key EMT-related molecules and pathways potentially modulated by NIEMFs, including VEGFR, ROS, P53, PI3K/AKT, MAPK, Cyclin B1, and NF-κB.

Main Results:

  • Evidence suggests that NIEMFs may influence EMT-related pathways, offering a potential mechanism for their anti-cancer effects.
  • Specific molecular targets like VEGFR, ROS, P53, PI3K/AKT, MAPK, Cyclin B1, and NF-κB are identified as potentially affected by NIEMFs.

Conclusions:

  • Understanding the interaction between NIEMFs and EMT pathways is crucial for developing novel anti-cancer therapies.
  • NIEMFs represent a promising area of research for targeting cancer metastasis through modulation of key cellular signaling pathways.

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