Abstract
Although BCR-ABL is the hallmark genetic abnormality of chronic myeloid leukemia (CML), secondary molecular events responsible for the evolution of the disease to blast crisis are yet to be deciphered. Taking into account the significant association of ecotropic viral integration site I (EVI1) in CML drug resistance, it is necessary to decipher the other roles played by EVI1 in CML disease progression. In this regard, we cross-hybridized three microarray datasets and deduced a set of 11 genes that seems to be regulated by EVI1 in CML. We observed a strong correlation between EVI1 and alpha1, 6-fucosyltransferase (FUT8) in the chronic phase of the disease and both of them were found to be up-regulated with the progression of the disease. Knockdown of EVI1 in a CML cell line not only down-regulated FUT8, but also rendered the cells towards erythroid differentiation. Our study shows the involvement of EVI1 and FUT8 axis in blocking erythropoiesis in CML.
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Acknowledgements
NK was supported by fellowship from the Indian Council of Medical Research (ICMR), India. KBN and SA were supported by fellowship from the Council of Scientific Industrial Research (CSIR), India. AH was supported by Inspire Fellowship, Department of Science and Technology (DST), India. The work was funded by the Institutional core grant.
Potential conflict of interest
Disclosure forms provided by the authors are available with the full text of this article online at http://dx.doi.org/10.1080/10428194.2016.1266622.