Acetylome and phosphoproteome modifications in imatinib resistant chronic myeloid leukaemia cells treated with valproic acid

被引：15

作者：

Buchi, Francesca ^{[1
]}

Pastorelli, Roberta ^{[2
]}

Ferrari, Germano ^{[1
]}

Spinelli, Elena ^{[1
]}

Gozzini, Antonella ^{[1
]}

Sassolini, Francesca ^{[1
]}

Bosi, Alberto ^{[1
]}

Tombaccini, Donatella ^{[2
]}

Santini, Valeria ^{[1
]}

机构：

[1] Univ Florence, Funct Unit Haematol, AUO Careggi, I-50134 Florence, Italy

[2] Univ Florence, Dept Expt Pathol & Oncol, I-50134 Florence, Italy

来源：

LEUKEMIA RESEARCH | 2011年 / 35卷 / 07期

关键词：

CML BCR/ABL; Proteomics; Imatinib resistance; Valproic acid; Protein phosphorylation; Protein acetylation; CHRONIC MYELOGENOUS LEUKEMIA; HISTONE DEACETYLASE INHIBITORS; TYROSINE KINASE INHIBITOR; BCR-ABL; STEM-CELLS; ANTILEUKEMIA ACTIVITY; K562; CELLS; APOPTOSIS; HEAT-SHOCK-PROTEIN-90; MESYLATE;

D O I：

10.1016/j.leukres.2011.01.033

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Chronic myeloid leukaemia has a specific therapy: BCR/ABL inhibitor imatinib. Resistance due to BCR/ABL dependent and independent mechanisms is partially reversible by histone deacetylase inhibitors. We analysed by 2D-electrophoresis and anti-pan-acetylated and anti-phosphotyrosine immunoblots, followed by spot-matching and MALDI-TOF mass spectrometry, which proteome modifications would parallel restoration of sensitivity to imatinib by valproic acid (VPA). VPA plus imatinib significantly increased acetylation of HSP90 and hnRNP L and decreased phosphorylation of HSPs and hnRNPs in imatinib resistant cells. VPA was able to modify profoundly acetylome and phosphoproteome of CML cells, while reverting resistance to imatinib. (C) 2011 Elsevier Ltd. All rights reserved.

引用

页码：921 / 931

页数：11

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