Literature DB >> 26493374

Bcl-2 phosphorylation confers resistance on chronic lymphocytic leukaemia cells to the BH3 mimetics ABT-737, ABT-263 and ABT-199 by impeding direct binding.

Ting Song1, Gaobo Chai2, Yubo Liu2, Xiaoyan Yu2, Ziqian Wang1, Zhichao Zhang1.   

Abstract

BACKGROUND AND
PURPOSE: Although the ongoing clinical trials of ABT-263 and ABT-199 in chronic lymphocytic leukaemia (CLL) have indicated that BH3 mimetics hold considerable promise, understanding the mechanism of CLL resistance to BH3 mimetics remains a challenge. EXPERIMENTAL APPROACH: The LD50 values of ABT-737, ABT-263 and ABT-199 in a number of primary CLL cells from 40 patients, were determined. The levels of Bcl-2 family proteins, including phosphorylated Bcl-2 (pBcl-2) and their interactions were measured by immunoblotting and co-immunoprecipitation. In vitro binding assays were performed by isothermal titration calorimetry and ELISA. BH3 profiling in isolated mitochondria was analysed. KEY
RESULTS: The ratio of (Mcl-1 + pBcl-2) to Bcl-2 expression provided the most significant predictive marker for the cytotoxic potential of ABT-737, ABT-263 and ABT-199 in the panel of CLL samples. Mechanistically, pBcl-2 inhibited the effects of the ABT compounds on the displacement of Bax and Bim from Bcl-2, thereby suppressing mitochondrial apoptosis. The ABT compounds exhibited 100-300-fold lower binding affinity to the glutamic acid, phosphomimetic, mutant of Bcl-2 (T69E, S70E and S87E; EEE-Bcl-2). BH3 peptides exhibited different rank orders of binding affinities to full-length WT-Bcl-2 and full-length EEE-Bcl-2. CONCLUSIONS AND IMPLICATIONS: Our study suggested that a structural alteration in the BH3-binding groove was induced by phosphorylation of Bcl-2. Our data also provided a framework to overcome resistance of CLL cells to the ABT compounds by combining pBcl-2 kinase inhibitors with the ABT compounds.
© 2015 The British Pharmacological Society.

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Year:  2016        PMID: 26493374      PMCID: PMC4728412          DOI: 10.1111/bph.13370

Source DB:  PubMed          Journal:  Br J Pharmacol        ISSN: 0007-1188            Impact factor:   8.739


  34 in total

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Authors:  D Westphal; R M Kluck; G Dewson
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Authors:  Andrew W Roberts; John F Seymour; Jennifer R Brown; William G Wierda; Thomas J Kipps; Seong Lin Khaw; Dennis A Carney; Simon Z He; David C S Huang; Hao Xiong; Yue Cui; Todd A Busman; Evelyn M McKeegan; Andrew P Krivoshik; Sari H Enschede; Rod Humerickhouse
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4.  Proteasomal degradation of human peptidyl prolyl isomerase pin1-pointing phospho Bcl2 toward dephosphorylation.

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Review 7.  Life in the balance: how BH3-only proteins induce apoptosis.

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Review 10.  Bim and Bmf in tissue homeostasis and malignant disease.

Authors:  J D Piñon; V Labi; A Egle; A Villunger
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  19 in total

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Review 2.  Found in Translation: How Preclinical Research Is Guiding the Clinical Development of the BCL2-Selective Inhibitor Venetoclax.

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Review 4.  The potential of venetoclax (ABT-199) in chronic lymphocytic leukemia.

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Journal:  Ther Adv Hematol       Date:  2016-07-08

5.  Selective ERBB2 and BCL2 Inhibition Is Synergistic for Mitochondrial-Mediated Apoptosis in MDS and AML Cells.

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8.  Mitochondrial PKM2 regulates oxidative stress-induced apoptosis by stabilizing Bcl2.

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9.  The BH3 mimetic drug ABT-737 induces apoptosis and acts synergistically with chemotherapeutic drugs in thyroid carcinoma cells.

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10.  Macitentan, a double antagonist of endothelin receptors, efficiently impairs migration and microenvironmental survival signals in chronic lymphocytic leukemia.

Authors:  Rossana Maffei; Stefania Fiorcari; Tiziana Vaisitti; Silvia Martinelli; Stefania Benatti; Giulia Debbia; Davide Rossi; Patrizia Zucchini; Leonardo Potenza; Mario Luppi; Gianluca Gaidano; Silvia Deaglio; Roberto Marasca
Journal:  Oncotarget       Date:  2017-09-27
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