Effects of radiofrequency radiation on colorectal cancer cell proliferation and inflammation

Author:

Ozgur Elcin1ORCID,Kayhan Handan2,Kismali Gorkem3,Senturk Fatih1ORCID,Sensoz Merve3,Ozturk Goknur Guler1,Sel Tevhide3

Affiliation:

1. Department of Biophysics , Faculty of Medicine, Gazi University , Ankara , Turkey

2. Department of Adult Hematology , Faculty of Medicine, Gazi University , Ankara , Turkey

3. Department of Biochemistry , Faculty of Veterinary Medicine, Ankara University , Ankara , Turkey

Abstract

Abstract Objectives 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. Methods 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. Results 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 cells. P53, p-P53, BAD, p-BAD, NF-κB, p-NF-κB, p-P38, p-SAPK/JNK, p-STAT3, and p-IkB levels increased after exposure to RFR at 900 and 2,100 MHz in DLD-1 cells. Unlike HCT-116 cells, 1,800 MHz of RFR was reported to have no effect on DLD1 cells. Conclusions RFR increased apoptosis and inflammatory response in HCT116 cells, 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.

Publisher

Walter de Gruyter GmbH

Subject

Biochemistry, medical,Clinical Biochemistry,Molecular Biology,Biochemistry

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