Effects of radiofrequency radiation on colorectal cancer cell proliferation and inflammation

Abstract

\n \n \n The aim of this study is to investigate the effects of radiofrequency radiation (RFR) on apoptosis, proliferation, stress response, and inflammation markers in colorectal cancer cells.\n \n \n \n We tested the effects of intermittent exposure to RFR at different frequencies on two different colorectal cancer cell lines; HCT-116 and DLD-1. Protein levels were subsequently analyzed by ELISA.\n \n \n \n RFR led to a decrease in P53, p-P53, p-P38, and p-IkB levels in HCT-116 cells, while leading to an increase in BAD, p-BAD, p-STAT3,NF-κB levels. Two thousand one hundred Megahertz of RFR altered the P53, BAD, and NF-ΚB expression in HCT-116\xa0cells. P53, p-P53, BAD, p-BAD, NF-κB, p-NF-κB, p-P38, p-SAPK/JNK, p-STAT3, and p-IkB\xa0levels increased after exposure to RFR at 900 and 2,100\xa0MHz in DLD-1\xa0cells. Unlike HCT-116\xa0cells, 1,800\xa0MHz of RFR was reported to have no effect on DLD1\xa0cells.\n \n \n \n RFR increased apoptosis and inflammatory response in HCT116\xa0cells, while lowering the active P38 and active P53 levels, which are indicators of poor prognosis in several cancers. Genetic differences, such as P53 mutation (DLD-1), are critical to the cell response to RFR, which explains the reason why scientific studies on the effects of RFR yield contradictory results.\n