Whole-genome gene expression comparison of the chronic myeloid leukemia cell line K562 and its tyrosine kinase inhibitor resistant subclone K562-IR.

The aim of the analysis is to study the relationship between tyrosine kinase inhibitor (TKI) resistance mechanism and phenotypic plasticity in the TKI-resistant and parental chronic myeloid leukemia K562 cell lines, in the presence and absence of imatinib. Results provide insight into the molecular mechanisms underlying the acquisition of cancer cell plasticity. 4 group of cell lines were studied in triplicate (12 samples) for the microarray analysis. K562 samples were used as reference. K562-IR w/ imatinib cells (suspension) and spindle-shape K562-IR cells (adhering under the suspension cells) were incubated continuously with 10µM imatinib. K562-IR w/o imatinib cells were centrifuged to remove imatinib, and then cultured in complete media during 4 week before collecting for the analysis. K562-IR w/ imatinib cells were collected directly using centrifugation, and spindle-shape K562-IR cells were trypsinized then collected by centrifugation because they grows as monolayer.