Flow solitons of supermolecular complex DEAE-dextran-MMA copolymer/small noncoding RNAs for epigenetic change from cancer to normal cells in TME

DDMC (DEAE-dextran-MMA copolymer)/sncRNAs (a-miR-155, piR-30074, and miR-125b) complex completely cured mice with virus-induced sarcoma after cellular reprogramming treatment, transforming cancer cells into normal cells. Comparing the kinetics of the control with tumor growth inhibition (mm²) - which involves one intravenous injection or two - shows the same curvature and speed, so it is a soliton wave with a permanent shape and speed, and in the case of two intravenous injections, a faster soliton overcomes another without any change in shape. The signal transduction for this drug delivery system (DDS) should be the Hill Sigmoid type following the nonlinear Schrodinger energy transfer model, the sine-Gordon soliton model for pulse and the Fisher-Kolmogorov soliton model for mass transfer. We found that the cellular output/entry response of DDMCs/sncRNAs is more dependent on the soliton signal not losing energy and shape without blocking communication. The soliton-induced endoplasmic reticulum-mitochondria Ca²⁺ fluxes in chromosomes in the nucleus create epigenetic modifications on the 5-position of cytosine (5mC) by Tet enzymes and thymine DNA glycosylase (TDG) as a global intracellular reaction. Quantum mechanical equations show that soliton flux can provide epigenetic control of Ca²⁺ fluxes using the "induced fit model" Hill equation.