High efficacy of the BCL-2 inhibitor ABT199 (venetoclax) in BCL-2 high-expressing neuroblastoma cell lines and xenografts and rational for combination with MCL-1 inhibition

被引:44
作者
Bate-Eya, Laurel T. [1 ]
den Hartog, Ilona J. M. [1 ]
van der Ploeg, Ida [1 ]
Schild, Linda [1 ]
Koster, Jan [1 ]
Santo, Evan E. [1 ]
Westerhout, Ellen M. [1 ]
Versteeg, Rogier [1 ]
Caron, Huib N. [2 ]
Molenaar, Jan J. [1 ]
Dolman, M. Emmy M. [1 ]
机构
[1] Univ Amsterdam, Dept Oncogen, Amsterdam, Netherlands
[2] Univ Amsterdam, Acad Med Ctr, Dept Pediat Oncol, Emma Kinderziekenhuis, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands
关键词
neuroblastoma; ABT199; BCL-2; MCL-1; resistance; OLIGOMERIZES BAK; LUNG-CANCER; ABT-199; FAMILY; NOXA; RESISTANCE; ABT-737; PROTEIN; DEATH; STABILITY;
D O I
10.18632/oncotarget.8547
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The anti-apoptotic protein B cell lymphoma/leukaemia 2 (BCL-2) is highly expressed in neuroblastoma and plays an important role in oncogenesis. In this study, the selective BCL-2 inhibitor ABT199 was tested in a panel of neuroblastoma cell lines with diverse expression levels of BCL-2 and other BCL-2 family proteins. ABT199 caused apoptosis more potently in neuroblastoma cell lines expressing high BCL-2 and BIM/BCL-2 complex levels than low expressing cell lines. Effects on cell viability correlated with effects on BIM displacement from BCL-2 and cytochrome c release from the mitochondria. ABT199 treatment of mice with neuroblastoma tumors expressing high BCL-2 levels only resulted in growth inhibition, despite maximum BIM displacement from BCL-2 and the induction of a strong apoptotic response. We showed that neuroblastoma cells might survive ABT199 treatment due to its acute upregulation of the anti-apoptotic BCL-2 family protein myeloid cell leukaemia sequence 1 (MCL-1) and BIM sequestration by MCL-1. In vitro inhibition of MCL-1 sensitized neuroblastoma cell lines to ABT199, confirming the pivotal role of MCL-1 in ABT199 resistance. Our findings suggest that neuroblastoma patients with high BCL-2 and BIM/BCL-2 complex levels might benefit from combination treatment with ABT199 and compounds that inhibit MCL-1 expression.
引用
收藏
页码:27946 / 27958
页数:13
相关论文
共 44 条
[11]   Targeting the B-Cell Lymphoma/Leukemia 2 Family in Cancer [J].
Davids, Matthew S. ;
Letai, Anthony .
JOURNAL OF CLINICAL ONCOLOGY, 2012, 30 (25) :3127-3135
[12]   Mitochondrial Bcl-2 Family Dynamics Define Therapy Response and Resistance in Neuroblastoma [J].
Goldsmith, Kelly C. ;
Gross, Michelle ;
Peirce, Susan ;
Luyindula, Dema ;
Liu, Xueyuan ;
Vu, Annette ;
Sliozberg, Michael ;
Guo, Rong ;
Zhao, Huaqing ;
Reynolds, C. Patrick ;
Hogarty, Michael D. .
CANCER RESEARCH, 2012, 72 (10) :2565-2577
[13]   Noxa up-regulation and Mcl-1 cleavage are associated to apoptosis induction by bortezomib in multiple myeloma [J].
Gomez-Bougie, Patricia ;
Wuilleme-Toumi, Soraya ;
Menoret, Emmanuelle ;
Trichet, Valerie ;
Robillard, Nelly ;
Philippe, Moreau ;
Bataille, Regis ;
Amiot, Martine .
CANCER RESEARCH, 2007, 67 (11) :5418-5424
[14]   Noxa controls Mule-dependent Mcl-1 ubiquitination through the regulation of the Mcl-1/USP9X interaction [J].
Gomez-Bougie, Patricia ;
Menoret, Emmanuelle ;
Juin, Philippe ;
Dousset, Christelle ;
Pellat-Deceunynck, Catherine ;
Amiot, Martine .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2011, 413 (03) :460-464
[15]   The pathophysiology of mitochondrial cell death [J].
Green, DR ;
Kroemer, G .
SCIENCE, 2004, 305 (5684) :626-629
[16]   Alterations in the Noxa/Mcl-1 axis determine sensitivity of small cell lung cancer to the BH3 mimetic ABT-737 [J].
Hauck, Paula ;
Chao, Bo H. ;
Litz, Julie ;
Krystal, Geoffrey W. .
MOLECULAR CANCER THERAPEUTICS, 2009, 8 (04) :883-892
[17]   Anticancer therapy targeting the apoptotic pathway [J].
Hu, W ;
Kavanagh, JJ .
LANCET ONCOLOGY, 2003, 4 (12) :721-729
[18]   BCL2 expression is a prognostic marker for the activated B-cell-like type of diffuse large B-cell lymphoma [J].
Iqbal, J ;
Neppalli, VT ;
Wright, G ;
Dave, LJ ;
Horsman, DE ;
Rosenwald, A ;
Lynch, J ;
Hans, CP ;
Weisenburger, DD ;
Greiner, TC ;
Gascoyne, RD ;
Campo, E ;
Ott, G ;
Müller-Hermelink, HK ;
Delabie, J ;
Jaffe, ES ;
Grogan, TM ;
Connors, JM ;
Vose, JM ;
Armitage, JO ;
Staudt, LM ;
Chan, WC .
JOURNAL OF CLINICAL ONCOLOGY, 2006, 24 (06) :961-968
[19]   Neuroblastoma Paradigm for Precision Medicine [J].
Irwin, Meredith S. ;
Park, Julie R. .
PEDIATRIC CLINICS OF NORTH AMERICA, 2015, 62 (01) :225-+
[20]   Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c [J].
Korsmeyer, SJ ;
Wei, MC ;
Saito, M ;
Weller, S ;
Oh, KJ ;
Schlesinger, PH .
CELL DEATH AND DIFFERENTIATION, 2000, 7 (12) :1166-1173