Residual expression of SMYD2 and SMYD3 is associated with the acquisition of complex karyotype in chronic lymphocytic leukemia

Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine
Wilson Oliveira-SantosFelipe Saldanha-Araujo

Abstract

SET and MYND domain containing 2 (SMYD2) and the SET and MYND domain containing 3 (SMYD3) are the most studied and well-characterized members of SMYD family. It has been demonstrated that their altered expression is associated with the progression of several solid tumors. Nevertheless, whether these methyltransferases exert any impact in chronic lymphocytic leukemia (CLL) remains unknown. Here, we investigated the gene expression profile of SMYD2 and SMYD3 in 59 samples of CLL and 10 normal B cells. The obtained results were associated with white blood cells (WBC) and platelet counts, ZAP-70 protein expression, and cytogenetic analysis. We found that SMYD2 and SMYD3 are overexpressed in CLL patients and, interestingly, patients with residual expression of both genes presented a high WBC count and complex karyotype. Furthermore, a strong correlation between SMYD2 and SMYD3 gene expression was unveiled. Our data demonstrate the association of a residual expression of SMYD2 and SMYD3 with CLL progression indicators and suggests both genes are regulated by a common transcriptional control in this type of cancer. These results may provide the basis for the development of new therapeutic strategies to prevent CLL progression.

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Citations

Aug 24, 2017·Environmental and Molecular Mutagenesis·Juliana Carvalho Alves-SilvaFelipe Saldanha-Araujo
Sep 28, 2018·Journal of Cellular Biochemistry·Cigir Biray AvciCumhur Gunduz
Jun 21, 2019·Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]·Fujia LinCaiwen Ou
Sep 24, 2016·Oncotarget·Sevgi BagislarBruno Amati
Aug 3, 2019·Clinical Epigenetics·Xin YiZe-Min Fang
Dec 27, 2016·Medical Science Monitor : International Medical Journal of Experimental and Clinical Research·Ting-Ting LiuQiong-Na Liu

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