To identify gene markers involved in EMT from EP156T to EPT1 cells, we profiled the gene expression of both cell lines using the Agilent Human Whole Genome Oligo Microarray, which contained 44 k probes.
The lowest level of detection of both cell lines using the EGFR and EphB4 markers was 5 cells per ml of peripheral blood.
As this cell line is known to exert high basal NFATc2 activity, in contrast to Panc1 cells, we next analysed the basal and the TRAIL-inducible NFAT activity in both cell lines, using the established NFAT/AP-1 binding site of the COX-2 promoter, by EMSA.
Indeed, following CHKA knockdown, a decreased proliferation was evident (see Figure 2B) and, as expected, a clear delay in wound closure was observed in both CHKA-silencing cell lines using the classic scratch assay.
Furthermore, for both lines, using CBV to predict the phenotype or hazard rate gave similar difference in survival days as the DBV (approximately 45 days for line W1 and 58 days for line WB).
When using a primer to exon 3, all of the transcripts characterized from both cell lines used the polyadenylation signal (UAUAAA), nearly identical to the consensus signal (AAUAAA), at approximately base 2060.
Although the signal differences between CD133-negative and -positive tumors were statistically significant for both pairs of cell lines used, the binding of the injected antibodies to their target still had to be confirmed.
After a thorough search of archives of public records, both printed and on-line, using the keywords leprosy and Hansen's disease, relevant documents were exhaustively collected from libraries, leprosaria/sanatoria, offices of patients' organizations, and the museum of Hansen's disease (Carville and Tokyo) in each country.
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