Title of article :
miR-155 effectively induces apoptosis in K562 Philadelphia positive cell line through upregulation of p27kip1
Author/Authors :
Sayadi Mahtab Hematology Department - School of Allied Medicine - Tehran University of Medical Sciences - Tehran, Iran , Edalati Fathabad Mahdi Hematology Department - School of Allied Medicine - Tehran University of Medical Sciences - Tehran, Iran , Alizadeh Shaban Hematology Department - School of Allied Medicine - Tehran University of Medical Sciences - Tehran, Iran , Karimipoor Morteza Molecular Medicine Department - Biotechnology Research Center - Pasteur Institute of Iran - Tehran, Iran , Abdoli Asghar Department of Hepatitis and AIDS - Pasteur Institute of Iran - Tehran, Iran , Atashi Amir Cancer Prevention Research Center - Shahroud University of Medical Sciences - Shahroud, Iran
Abstract :
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.
Keywords :
Apoptosis , K562 , miR-155 , Philadelphia , p27kip1
Journal title :
Bioimpacts