Increased Expression of Tubulin A, Cyclin B1, and Ki67 May Associate with Cell Death Mechanism Caused by Noncontact Electro Capacitive Cancer Exposure in vitro
Keywords:ECCT; in vitro; cell death; Tubulin A; Cyclin B1; Ki-67; mitotic arrest
Background: Noncontact Electro Capacitive Cancer Therapy (ECCT) is a novel treatment modality in
cancer that uses low-intensity intermediate-frequency alternating electric field. A previous study has reported
ECCT could induce cell death in cancer cells, but the molecular mechanism underlining this process remains
unclear. Therefore, this study aims to uncover the molecular mechanisms of the pathology induced by the
device and to determine whether Tubulin A, Cyclin B, and Ki67 can serve as biomarkers for this exposure.
Methods: This study was an in vitro laboratory experiment with Completely Randomized Block Design.
Two different types of cancerous cell lines were used in this study: oral squamous cell carcinomas and Hela
cells. In addition, non-cancerous cell line, bone marrow mesenchymal cell, was also subjected to the electric
field produced by ECCT. All three cell lines were divided into two groups: the ECCT-exposed group and
the control group. After exposure, the protein expression of Tubulin A, Cyclin B, and Ki-67 was examined
using immunocytochemistry staining.
Results: The results showed that the number of Tubulins A, Cyclin B1, and Ki-67 expression was
significantly higher in ECCT-exposed group than in the control group (p<0.05). Increased expression of
tubulin A indicates a disruption to microtubule polymerization, an increase in Cyclin B expression indicates
mitotic arrest or incomplete mitosis, whereas the increase of Ki-67 expression occurs when cells stop in the
metaphase phase (mitotic arrest).
Conclusion: It could be concluded that increased Tubulins A, Cyclin B1, and Ki-67 expression may associate
with the death cell mechanism induced by exposure to Noncontact Electro Capacitive Cancer devise.
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