Cyclic Electromagnetic DNA Simulation (CEDS) targeting Telomere Repeat Sequence can enhance Anticancer Effect, while CEDS targeting Canonical E-box Sequence induce Oncogenic Effect in Cells

Abstract

Cyclic electromagnetic DNA simulation (CEDS) was used in the previous study (1) to stimulate the base pair polarities of oligo-dsDNAs, plasmid DNAs, and miRNAs. This study applied dodecagonal CEDS to target telomere repeat sequence (TTAGGG*-CEDS), canonical E-box sequence (CACGTG*-CEDS) in genomic DNA of RAW 264.7 cells and KB cells. During cell culture, CEDS was performed at 20-25 Gauss for 20 min, and followed by cytological observation and immunoprecipitation high-performance liquid chromatography (IP-HPLC) using 350 antisera. KB cells treated with TTAGGG*-CEDS showed a significant decrease in cell density and metachromasia in toluidine blue staining compared to untreated control, while only a slight decrease in cell density and metachromasia was observed by telomere mutation sequence, TTTGGG*-CEDS. Conversely, CACGTG*-CEDS induced almost no change in cell density, cell number, metachromasia in toluidine blue staining compared to random sequence*-CEDS (2(ACGT)*-CEDS) and untreated control. IP-HPLC results showed that TTAGGG*-CEDS induced a potent anticancer effect by downregulating RAS, oncogenesis, and telomere signaling, and activating NFkB signaling-p53-and FAS-mediated apoptosis-innate and cellular immunity signaling axis compared to untreated control and positive control performed with nonspecific poly-A 12A*-CEDS. In contrast, CACGTG*-CEDS exhibited a significant oncogenic effect by enhancing of RAS and NFkB signaling and resulting oncogenesis-glycolysis-chronic inflammation signaling axis. Therefore, it is suggested that CEDS is able to target DNA motif sequences in genomic DNA, and that TTAGGG*-CEDS and CACGTG*-CEDS are favorable candidates to regulate important genes involved in oncogenesis, inflammation, apoptosis, etc.