BCR-ABL1-associated reduction of beta catenin antagonist Chibby1 in chronic myeloid leukemia

PloS One
Elisa LeoGiovanni Martinelli

Abstract

Beta Catenin signaling is critical for the self-renewal of leukemic stem cells in chronic myeloid leukemia. It is driven by multiple events, enhancing beta catenin stability and promoting its transcriptional co-activating function. We investigated the impact of BCR-ABL1 on Chibby1, a beta catenin antagonist involved in cell differentiation and transformation. Relative proximity of the Chibby1 encoding gene (C22orf2) on chromosome 22q12 to the BCR breakpoint (22q11) lets assume its involvement in beta catenin activation in chronic myeloid leukemia as a consequence of deletions of distal BCR sequences encompassing one C22orf2 allele. Forty patients with chronic myeloid leukemia in chronic phase were analyzed for C22orf2 relocation and Chibby1 expression. Fluorescent in situ hybridization analyses established that the entire C22orf2 follows BCR regardless of chromosomes involved in the translocation. In differentiated hematopoietic progenitors (bone marrow mononuclear cell fractions) of 30/40 patients, the expression of Chibby1 protein was reduced below 50% of the reference value (peripheral blood mononuclear cell fractions of healthy persons). In such cell context, Chibby1 protein reduction is not dependent on C22orf2 transcripti...Continue Reading

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Jan 21, 2017·Cell Cycle·Victoria FischerKen-Ichi Takemaru
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Apr 13, 2017·Journal of Cellular Biochemistry·Manuela ManciniGiovanni Martinelli

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Methods Mentioned

BETA
density gradient centrifugation
PCR
ubiquitination
acetylation
glycosylation

Clinical Trials Mentioned

NCT00769327
NCT01535391
NCT01061177

Software Mentioned

Genikon
IMAGEJ

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