Altered apoptotic protein expressions characterize the survival of Bcr-Abl-independent drug-resistant chronic myeloid leukemia cell line

Abstract

Apoptosis is a programmed cellular process that occurs in pathological and physiological pathways and it is one of the most studied topics in cell biology. To understand the underlying mechanism of apoptosis plays an important role in the molecular pathogenesis of many diseases including cancers. Chronic myeloid leukemia (CML) is a clonal myeloproliferative malignancy arising from the neoplastic transformation of the hematopoietic stem cell. Here, we used a Bcr-Abl-independent, imatinib-resistant K562 subpopulation (K562-IR) generated and characterized earlier in our laboratory. We showed that the proteins Bcl-2, Bim, RIP, p-MAPK(Erk1/Erk2) and NF-кB which play critical roles in cell death pathways are downregulated, Lamin A/C protein expression is upregulated in K562-IR derivative cells compared to K562 ancestral cells. Our data provide new information on the expression of apoptotic molecules in a Bcr-Abl-independent imatinib-resistant CML cell line.

Keywords

• chronic myeloid leukemia
• apoptosis
• Bcl-2
• Bim
• RIP
• NFkB

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