Hexavalent chromium induces γH2AX and RAD51 involved in DNA damage repair in BEAS-2B cells by modulating LNC-DHFR-4:1

Abstract

Hexavalent chromium [Cr(VI)] is rarely found in nature. Its occurrence in the environment is mainly due to anthropogenic sources. Our previous studies have shown that Cr(VI) exposure could change the expression profile of long noncoding RNAs (lncRNAs). However, the relationship between lncRNAs and genetic damage induced by Cr(VI) remains unclear. In this study, RT–qPCR was used to verify the expression of genes and lncRNAs involved in DNA damage repair in BEAS-2B cells exposed to different Cr(VI) concentrations. After screening out LNC-DHFR-4:1, overexpression and knockdown models of BEAS-2B cells were used to further identify the relationship between the lncRNA and RAD51. RT–qPCR and indirect immunofluorescence were used to detect expression. Our results revealed that with increasing Cr(VI) concentration, γH2AX expression was increased, while the expression of RAD51 was decreased. Meanwhile, LNC-DHFR-4:1 acted as a competitive endogenous RNA to regulate the expression of γH2AX and RAD51, which further affected DNA damage repair. The overexpression of LNC-DHFR-4:1 induced a twofold decrease in γH2AX and a onefold increase in RAD51, and its knockdown showed the opposite results. These results suggested that LNC-DHFR-4:1 might be a potential biomarker of Cr(VI)-induced DNA damage repair in BEAS-2B cells.

Keywords

• Hexavalent chromium
• Human bronchial epithelial cell line
• Long noncoding RNA
• DNA damage repair
• Biomarker