HEK293 cell and 293 sublineage cells (Epstein-Barr virus (EBV) latent infection) Genome sequencing. Homo sapiens

Epstein-Barr virus (EBV) latent infection facilitated the tumorigenicity was previously established using the Maxi-EBV system. The LMP1 gene in Maxi-EBV genome was replaced by that of nasopharyngeal carcinoma origin. By using the Maxi-EBV system and immortalized 293 epithelial cell line with low malignancy, we previously developed the cell line 293-EBV, and established a tumor model in nude mice.The cell line 293–1/NL with the replacement of N-LMP1(21 strains of full-lenthLMP1 genes of NPC origin) in EBV genome showed much lower tumorigenicity than the original 293-EBV cell lineThe resultant cell line, 293–1/NL showed much lowermalignancy than the original 293-EBV. The result was opposite to our expectation. The change of 293 sublineage cells for EBV harboring also got similar result. To seek the underlying reason, the copy number of EBV genome in all the cell lines was detected. The result indicated that 293-EBV contained about 4.5-fold higher EBV copies than 293–1/NL did. Parallel EBV genomes led to relatively stable copies in different 293 sublineages, suggesting the viral genome structure is a factor for the sustainability of EBV’s copy number. The sub-lineage 293–2 has a higher ability to form tumors in nude mice than 293–1. In order to verify above result for N-LMP1 in genome analysis, these two EBV genomes containing B-LMP1 (wildtype B95–8 strain) or N-LMP1 were introduced into 293–2 cells respectively. Two cell lines, C2089 and C22, were accordingly produced after hygromycin selection process . As shown in the tumor formation test , from the tumor growth sizes within 5 weeks,C22 also showed lower malignancy than C2089.