Increased Expression of Tubulin A, Cyclin B1, and Ki67 May Associate with Cell Death Mechanism Caused by Noncontact Electro Capacitive Cancer Exposure in vitro

Abstract

Background: Noncontact Electro Capacitive Cancer Therapy (ECCT) is a novel treatment modality incancer that uses low-intensity intermediate-frequency alternating electric field. A previous study has reportedECCT could induce cell death in cancer cells, but the molecular mechanism underlining this process remainsunclear. Therefore, this study aims to uncover the molecular mechanisms of the pathology induced by thedevice 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 Helacells. In addition, non-cancerous cell line, bone marrow mesenchymal cell, was also subjected to the electricfield produced by ECCT. All three cell lines were divided into two groups: the ECCT-exposed group andthe control group. After exposure, the protein expression of Tubulin A, Cyclin B, and Ki-67 was examinedusing immunocytochemistry staining.Results: The results showed that the number of Tubulins A, Cyclin B1, and Ki-67 expression wassignificantly higher in ECCT-exposed group than in the control group (p<0.05). Increased expression oftubulin A indicates a disruption to microtubule polymerization, an increase in Cyclin B expression indicatesmitotic arrest or incomplete mitosis, whereas the increase of Ki-67 expression occurs when cells stop in themetaphase phase (mitotic arrest).Conclusion: It could be concluded that increased Tubulins A, Cyclin B1, and Ki-67 expression may associatewith the death cell mechanism induced by exposure to Noncontact Electro Capacitive Cancer devise.