Electric Fields Regulate In Vitro Surface Phosphatidylserine Exposure of Cancer Cells via a Calcium-Dependent Pathway

Cancer is the second leading cause of death worldwide after heart disease. The current treatment options to fight cancer are limited, and there is a critical need for better treatment strategies. During the last several decades, several electric field (EF)-based approaches for anti-cancer therapies...

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Published in:Biomedicines 2023-02, Vol.11 (2), p.466
Main Authors: Kaynak, Ahmet, N'Guessan, Kombo F, Patel, Priyankaben H, Lee, Jing-Huei, Kogan, Andrei B, Narmoneva, Daria A, Qi, Xiaoyang
Format: Article
Language:English
Subjects:
Actin
Antibiotics
Antigens
Astrocytes
Biomarkers
Calcium (intracellular)
calcium modulation
cancer biomarker
Cancer cells
Cancer therapies
Cell culture
Cell cycle
Cell surface
electric field
Electric fields
Electroporation
enhanced cancer therapy
Glioblastoma
Health aspects
Heart diseases
Kinases
MAP kinase
Microscopy
p38 MAPK-actin pathway
Pancreatic cancer
Phosphatidylserine
Radiation
surface phosphatidylserine exposure
Tumor cell lines
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Summary:Cancer is the second leading cause of death worldwide after heart disease. The current treatment options to fight cancer are limited, and there is a critical need for better treatment strategies. During the last several decades, several electric field (EF)-based approaches for anti-cancer therapies have been introduced, such as electroporation and tumor-treating fields; still, they are far from optimal due to their invasive nature, limited efficacy and significant side effects. In this study, we developed a non-contact EF stimulation system to investigate the in vitro effects of a novel EF modality on cancer biomarkers in normal (human astrocytes, human pancreatic ductal epithelial -HDPE-cells) and cancer cell lines (glioblastoma U87-GBM, human pancreatic cancer cfPac-1, and MiaPaCa-2). Our results demonstrate that this EF modality can successfully modulate an important cancer cell biomarker-cell surface phosphatidylserine (PS). Our results further suggest that moderate, but not low, amplitude EF induces p38 mitogen-activated protein kinase (MAPK), actin polymerization, and cell cycle arrest in cancer cell lines. Based on our results, we propose a mechanism for EF-mediated PS exposure in cancer cells, where the magnitude of induced EF on the cell surface can differentially regulate intracellular calcium (Ca ) levels, thereby modulating surface PS exposure.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines11020466