LncRNA expression profiling and its relationship with DNA damage in Cr(VI)-treated 16HBE cells

Compounds containing hexavalent chromium [Cr(VI)] were Group I human carcinogens which were mutagenic and can induce DNA damage. Cr(VI) exposure could cause a lot of changes in mRNA, protein and microRNA expression as well as DNA methylation. There were still few studies on the role of long non-coding RNA (lncRNA) in the carcinogenic process of Cr(VI). In current study, lncRNA expression profiling and bioinformatics analysis in 16HBE cells treated by Cr(VI) were performed. The cell counting kit-8 (CCK-8) assay and the comet assay were done to assess the cell viability and DNA damage in Cr(VI)-treated 16HBE cells respectively. The lncRNA expression profile was performed by Arraystar Microarray V3.0 in 16HBE cells treated with 0.00 and 10.00 μmol/L Cr(VI). Real-time quantitative polymerase chain reaction (RT-qPCR) was applied to verify some significantly altered lncRNAs. Gene ontology (GO), kyoto encyclopedia of genes and genomes (KEGG) analysis and mRNA-lncRNA network analysis were conducted to identify related biological processes, signal pathway and critical lncRNAs. It was found that Cr(VI) could induce cells viability decline and alter lncRNA expression profile of 16HBE cells. 1868 lncRNAs were significantly up-regulated and 2203 lncRNAs were significantly down-regulated which formed a complex regulation network. With the increase of Cr(VI) concentration, some lncRNAs increased or decreased gradually. The differentially expressed LncRNA profiling induced by Cr(VI) were associated with immune response, cell cycle, DNA damage and repair and so on. RP11-388M20.9 and AC092620.3 were nonlinearly decreasing with the change of the DNA content of comet tails (Tail DNA), tail length (TLL), tail moment (TM) and Olive Tail Moment (OTM), and the fitting results of Tail DNA and TM were statistically significant (P < 0.05). It was possible for RP11-388M20.9 to regulate DNA damage by interacting with the target gene after Cr(VI) exposure, and was likely to be a potential biomarker of DNA damage in Cr(VI)-treated 16HBE cells.