Traditional drug development and pre-clinical tests are based on animals and involve large numbers of animals,costs and long periods. Meanwhile,inter-species differences are difficult to overcome. Human embryonic stem cells (hESCs),which can self-renew and directly differentiate to types of cells,have become a new tool for toxicity alternative testing. hESC-Based alternative testing models,such as the reproductive toxicity test system,neuro development toxicity test system and metabolic model,can be used to predict target organ toxicity and toxic mechanisms of chemicals, analyze metabolic pathways and to search for potential toxicity biomarkers, when combined with omics such techiniques as metabonomics , proteomics and genomics. Therefore, hESC-based alternative testing models have extensive application to toxicology.

Objective: To investigate the expression and role of LINC00052 during glycidyl methacrylate (GMA) -induced malignant transformation of 16HBE cells. Methods: Human bronchial epithelial (16HBE) cells were divided into GMA transformation group and corresponding DMSO control group, and the 10th, 20th and 30th generation cells of each group were collected LncRNA microarrays were used to analysis expression of LINC00052 in different stage of malignant transformation. Bioinformatics analysis was applied and the relative expression of LINC00052 and its potentially target genes was detected by real-time quantification PCR (qPCR) . Results: The results of microarray analysis showed that LINC00052 was up-regulated by 1.32-fold, down-regulated by 1.64-fold and down-regulated by 4.92-fold in the malignant transformation early (P10) , middle term (P20) and late (P30) , respectively, The results of qPCR showed that compared with the DMSO control group, the expression of LINC00052 was up-regulated by 1.55 times, down-regulated by 1.20 times and down-regulated by 2.35 times in P10, P20 and P30, respectively, and the difference was statistically significant (P<0.05) . There was a statistically significant difference in the relative expression of NTRK3 between the GMA transformation group of P10 and P30 generations with the corresponding DMSO control group (P<0.05) . Conclusion LINC00052 is highly expressed in early time of GMA-induced malignant transformation of 16HBE, and down-regulated in the middle and last stage of malignant transformation and may play a protective role in GMA-induced malignant transformation of 16HBE by influencing the expression of its target gene NTRK3.