| Abstract
Introduction: Chronic myelogenous
leukemia (CML) is a myeloproliferative
disorder caused by the Philadelphia
chromosome translocation, at (9; 22),
which results in BCR-ABL fusion tyrosine
kinase oncoprotein. This fusion induces
down-regulation of miR-155. Upregulation
of miR-155 can influence cell fate via the
effect on p27kip1 and apoptosis. The aim
of this study was to induce apoptosis in
K562 CML cell line by overexpression of
miR-155.
Methods: The K562 cell line was transfected with pLenti-III-pre mir155-GFP constructs through
electroporation. Then, overexpression of miR-155 as well as the expression level of p27kip1 and
c-Myc was analyzed by quantitative PCR (qPCR). The level of p27 (Kip1) protein expression was
measured by Western blot and the Annexin V method was carried out to investigate apoptosis.
Results: Flow cytometric analysis results of K562 cells transfected with pLenti-III-pre mir155-
GFP construct showed a significant increase in cell apoptosis. Gene expression and protein level
of p27kip1 were upregulated. However, there was no change in c-Myc expression profile.
Conclusion: miR-155 could be a promising approach to aid in the treatment of CML. However,
further studies are required in this respect. |