Response of neuroblastoma cells to RF currents as a function of the signal frequency

Autor: Raquel Roldán, Alejandro Úbeda, Enrique Medel, María Luisa Hernández-Bule, Clara Colastra
Rok vydání: 2019
Předmět:
0301 basic medicine
Cancer Research
Programmed cell death
Electrothermal therapy
Cell Survival
MAP Kinase Signaling System
Apoptosis
lcsh:RC254-282
Neuroblastoma
03 medical and health sciences
0302 clinical medicine
Electric currents
Subthermal
Cell Line
Tumor
Genetics
Humans
Cyclin D1
Viability assay
Receptor
Cell Proliferation
bcl-2-Associated X Protein
Flavonoids
Cytostasis
Caspase 3
Cell growth
Chemistry
Cell Cycle Checkpoints
Cell cycle
lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
Capacitive-resistive electric transfer
Pulsed Radiofrequency Treatment
Cell biology
ErbB Receptors
030104 developmental biology
Oncology
Neural Crest
030220 oncology & carcinogenesis
NB69
Cancer cell
Tumor Suppressor Protein p53
Cyclin-Dependent Kinase Inhibitor p27
Signal Transduction
Research Article
Zdroj: BMC Cancer
BMC Cancer, Vol 19, Iss 1, Pp 1-14 (2019)
ISSN: 1471-2407
DOI: 10.1186/s12885-019-6090-6
Popis: Background Capacitive-resistive electric transfer (CRET) is a non-invasive therapeutic strategy that applies radiofrequency electric currents within the 400–600 kHz range to tissue repair and regeneration. Previous studies by our group have shown that 48 h of intermittent exposure to a 570 kHz CRET signal at a subthermal density of 50 μA/mm2 causes significant changes in the expression and activation of cell cycle control proteins, leading to cycle arrest in human cancer cell cultures. The present study investigates the relevance of the signal frequency in the response of the human neuroblastoma cell line NB69 to subthermal electric treatment with four different signal frequency currents within the 350–650 kHz range. Methods Trypan blue assay, flow cytometry, immunofluorescence and immunoblot were used to study the effects of subthermal CRET currents on cell viability, cell cycle progression and the expression of several marker proteins involved in NB69 cell death and proliferation. Results The results reveal that among the frequencies tested, only a 448 kHz signal elicited both proapoptotic and antiproliferative, statistically significant responses. The apoptotic effect would be due, at least in part, to significant changes induced by the 448 kHz signal in the expression of p53, Bax and caspase-3. The cytostatic response was preceded by alterations in the kinetics of the cell cycle and in the expression of proteins p-ERK1/2, cyclin D1 and p27, which is consistent with a potential involvement of the EGF receptor in electrically induced changes in the ERK1/2 pathway. This receives additional support from results indicating that the proapototic and antiproliferative responses to CRET can be transiently blocked when the electric stimulus is applied in the presence of PD98059, a chemical inhibitor of the ERK1/2 pathway. Conclusion The understanding of the mechanisms underlying the ability of slowing down cancer cell growth through electrically-induced changes in the expression of proteins involved in the control of cell proliferation and apoptosis might afford new insights in the field of oncology.
Databáze: OpenAIRE
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