The K562 chronic myeloid leukemia cell line undergoes apoptosis in response to interferon-alpha.
OBJECTIVE
The K562 cell line, derived from a chronic myeloid leukemia (CML) patient and expressing B3A2 bcr-abl hybrid gene, is known to be particularly resistant to apoptotic death. IFN-alpha treatment of CML patients impairs malignant cell clone, apparently protecting from progression to terminal blast crisis. The mechanisms underlying this kind of cell deletion are analyzed here by multiple technical approaches.


METHODS
K562 cells, variably treated with IFN-alpha, were examined by agarose gel DNA electrophoresis, light and electron microscopy. The presence of bcr-abl rearrangement was revealed by RT-PCR.


RESULTS
At 4 day treatment both DNA ladder and apoptotic nuclear changes were identified, consistently in the presence of bcr-abl expression.


CONCLUSIONS
Even cells expressing bcr-abl, such as K562, can be triggered to apoptosis. Therefore, this genetic condition, commonly preventing PCD, does not prevent IFN-alpha-mediated apoptosis. PCD seems thus to be the mechanism underlying IFN-alpha-treated K562 cell deletion and it could be the basis of malignant clone reduction in IFN-alpha treated CML patients.
Luchetti
F
F
Istituto di Scienze Morfologiche, Università di Urbino, Italy.
Gregorini
A
A
Papa
S
S
Burattini
S
S
Canonico
B
B
Valentini
M
M
Falcieri
E
E
D017209:Apoptosis / Q000187:drug effects*; D014408:Biomarkers, Tumor / Q000032:analysis; D053938:DNA Fragmentation; D004273:DNA, Neoplasm / Q000032:analysis; D016044:Fusion Proteins, bcr-abl / Q000032:analysis; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000494:pharmacology*; D020014:K562 Cells / Q000187:drug effects*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000473:pathology; D011994:Recombinant Proteins
D014408:Biomarkers, Tumor; D004273:DNA, Neoplasm; D007155:Immunologic Factors; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D016044:Fusion Proteins, bcr-abl