The role of boric acid on endoplasmic reticulum stress in human lung epithelial cells and lung cancer cells

Aim: Research Does boric acid activate the ER stress pathway in lung epithelial cells and lung cancer cell models? It is aimed to investigate the role of boric acid on ER stress and to determine protein and mRN expression by using Western Blot and RT-qPCR technique. Material and Method: A549 and BEAS2B cells were used as models in this study. In this direction, the amount of boric acid suitable for the study was determined by MTT analysis. Following this study, RNA and protein isolations were made by applying boric acid to cells cultured under appropriate conditions, and RT-PCR and Western Blot analysis tests were performed. Results: Gene expression levels of genes involved in the ER stress pathway (PERK, XBP1, MAOA, ATF6) were compared by performing relative quantitative analyzes and Student's T test. In PERK, XBP1 genes, there was a statistically significant difference with p<0.05 values in which boric acid triggered apoptosis in response to ER stress-induced UPR (PERK p1=0.000488 p2=0.000977, XBP1 p1=0.000253 p2=0.000506), while MAOA and ATF6 stress-induced excessive gene expression was not detected (MAOA p1=0.450321203 p2=0.900642405, ATF6 p1=0.496131 p2=0.992261). In immunoblotting analyzes, it was seen that protein level analyzes in PERK and XBP1 supported the results of RT-PCR analysis when compared to the control. There was no significant difference similar to PCR results for ATF6 and MAOA. A significant difference was observed in the immunoblotting analysis compared to the MAOA, RT-PCR analysis result. Conclusion: As a result of the analyzes, boric acid treatment of A549 and BEAS2B cells increased ER stress compared to the control, accordingly, a significant difference was observed in PERK, XBP1 and MAOA, but no significant difference was observed in ATF6. Key words: ATF6, Boron toxicity, Endoplasmic Reticulum(ER) stress, Real Time qPCR, Western blot