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Article ; Online: Longitudinal evaluation of serum microRNAs as biomarkers for neuroblastoma burden and therapeutic p53 reactivation.

Van Goethem, Alan / Deleu, Jill / Yigit, Nurten / Everaert, Celine / Moreno-Smith, Myrthala / Vasudevan, Sanjeev A / Zeka, Fjoralba / Demuynck, Fleur / Barbieri, Eveline / Speleman, Frank / Mestdagh, Pieter / Shohet, Jason / Vandesompele, Jo / Van Maerken, Tom

NAR cancer

2023 Volume 5, Issue 1, Page(s) zcad002

Abstract: Accurate assessment of treatment response and residual disease is indispensable for the evaluation of cancer treatment efficacy. However, performing tissue biopsies for longitudinal follow-up poses a major challenge in the management of solid tumours ... ...

Abstract	Accurate assessment of treatment response and residual disease is indispensable for the evaluation of cancer treatment efficacy. However, performing tissue biopsies for longitudinal follow-up poses a major challenge in the management of solid tumours like neuroblastoma. In the present study, we evaluated whether circulating miRNAs are suitable to monitor neuroblastoma tumour burden and whether treatment-induced changes of miRNA abundance in the tumour are detectable in serum. We performed small RNA sequencing on longitudinally collected serum samples from mice carrying orthotopic neuroblastoma xenografts that were exposed to treatment with idasanutlin or temsirolimus. We identified 57 serum miRNAs to be differentially expressed upon xenograft tumour manifestation, out of which 21 were also found specifically expressed in the serum of human high-risk neuroblastoma patients. The murine serum levels of these 57 miRNAs correlated with tumour tissue expression and tumour volume, suggesting potential utility for monitoring tumour burden. In addition, we describe serum miRNAs that dynamically respond to p53 activation following treatment of engrafted mice with idasanutlin. We identified idasanutlin-induced serum miRNA expression changes upon one day and 11 days of treatment. By limiting to miRNAs with a tumour-related induction, we put forward hsa-miR-34a-5p as a potential pharmacodynamic biomarker of p53 activation in serum.
Language	English
Publishing date	2023-01-18
Publishing country	England
Document type	Journal Article
ISSN	2632-8674
ISSN (online)	2632-8674
DOI	10.1093/narcan/zcad002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Anti-Tumor Activity of the NEDD8 Inhibitor Pevonedistat in Neuroblastoma.

Foster, Jennifer H / Barbieri, Eveline / Zhang, Linna / Scorsone, Kathleen A / Moreno-Smith, Myrthala / Zage, Peter / Horton, Terzah M

International journal of molecular sciences

2021 Volume 22, Issue 12

Abstract: Pevonedistat is a neddylation inhibitor that blocks proteasomal degradation of cullin-RING ligase (CRL) proteins involved in the degradation of short-lived regulatory proteins, including those involved with cell-cycle regulation. We determined the ... ...

Abstract	Pevonedistat is a neddylation inhibitor that blocks proteasomal degradation of cullin-RING ligase (CRL) proteins involved in the degradation of short-lived regulatory proteins, including those involved with cell-cycle regulation. We determined the sensitivity and mechanism of action of pevonedistat cytotoxicity in neuroblastoma. Pevonedistat cytotoxicity was assessed using cell viability assays and apoptosis. We examined mechanisms of action using flow cytometry, bromodeoxyuridine (BrDU) and immunoblots. Orthotopic mouse xenografts of human neuroblastoma were generated to assess in vivo anti-tumor activity. Neuroblastoma cell lines were very sensitive to pevonedistat (IC50 136-400 nM). The mechanism of pevonedistat cytotoxicity depended on p53 status. Neuroblastoma cells with mutant (p53
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cyclopentanes/pharmacology ; Cyclopentanes/therapeutic use ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Humans ; Mice ; NEDD8 Protein/antagonists & inhibitors ; NEDD8 Protein/metabolism ; Neuroblastoma/drug therapy ; Pyrimidines/pharmacology ; Pyrimidines/therapeutic use ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Antineoplastic Agents ; Cyclopentanes ; Enzyme Inhibitors ; NEDD8 Protein ; NEDD8 protein, human ; Pyrimidines ; Tumor Suppressor Protein p53 ; pevonedistat (S3AZD8D215)
Language	English
Publishing date	2021-06-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22126565
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Article ; Online: The Anti-Tumor Activity of the NEDD8 Inhibitor Pevonedistat in Neuroblastoma

Jennifer H. Foster / Eveline Barbieri / Linna Zhang / Kathleen A. Scorsone / Myrthala Moreno-Smith / Peter Zage / Terzah M. Horton

International Journal of Molecular Sciences, Vol 22, Iss 6565, p

2021 Volume 6565

Abstract: Pevonedistat is a neddylation inhibitor that blocks proteasomal degradation of cullin–RING ligase (CRL) proteins involved in the degradation of short-lived regulatory proteins, including those involved with cell-cycle regulation. We determined the ... ...

Abstract	Pevonedistat is a neddylation inhibitor that blocks proteasomal degradation of cullin–RING ligase (CRL) proteins involved in the degradation of short-lived regulatory proteins, including those involved with cell-cycle regulation. We determined the sensitivity and mechanism of action of pevonedistat cytotoxicity in neuroblastoma. Pevonedistat cytotoxicity was assessed using cell viability assays and apoptosis. We examined mechanisms of action using flow cytometry, bromodeoxyuridine (BrDU) and immunoblots. Orthotopic mouse xenografts of human neuroblastoma were generated to assess in vivo anti-tumor activity. Neuroblastoma cell lines were very sensitive to pevonedistat (IC50 136–400 nM). The mechanism of pevonedistat cytotoxicity depended on p53 status. Neuroblastoma cells with mutant (p53 MUT ) or reduced levels of wild-type p53 (p53si-p53) underwent G2-M cell-cycle arrest with rereplication, whereas p53 wild-type (p53 WT ) cell lines underwent G0-G1 cell-cycle arrest and apoptosis. In orthotopic neuroblastoma models, pevonedistat decreased tumor weight independent of p53 status. Control mice had an average tumor weight of 1.6 mg + 0.8 mg versus 0.5 mg + 0.4 mg ( p < 0.05) in mice treated with pevonedistat. The mechanism of action of pevonedistat in neuroblastoma cell lines in vitro appears p53 dependent. However, in vivo studies using mouse neuroblastoma orthotopic models showed a significant decrease in tumor weight following pevonedistat treatment independent of the p53 status. Novel chemotherapy agents, such as the NEDD8-activating enzyme (NAE) inhibitor pevonedistat, deserve further study in the treatment of neuroblastoma.
Keywords	pevonedistat ; cell cycle ; xenograft ; rereplication ; cullin–ring ligase ; ubiquitination ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616 ; 572
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Editor's Note: Dopamine Blocks Stress-mediated Ovarian Carcinoma Growth.

Moreno-Smith, Myrthala / Lu, Chunhua / Shahzad, Mian M K / Pena, Guillermo N Armaiz / Allen, Julie K / Stone, Rebecca L / Mangala, Lingegowda S / Han, Hee Dong / Kim, Hye Sun / Farley, Donna / Berestein, Gabriel Lopez / Cole, Steve W / Lutgendorf, Susan K / Sood, Anil K

Clinical cancer research : an official journal of the American Association for Cancer Research

2021 Volume 27, Issue 15, Page(s) 4451

Language	English
Publishing date	2021-07-24
Publishing country	United States
Document type	Journal Article ; Expression of Concern
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-21-2117
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Article ; Online: MYCN-driven fatty acid uptake is a metabolic vulnerability in neuroblastoma.

Nature communications

2022 Volume 13, Issue 1, Page(s) 3728

Abstract: Neuroblastoma (NB) is a childhood cancer arising from sympatho-adrenal neural crest cells. MYCN amplification is found in half of high-risk NB patients; however, no available therapies directly target MYCN. Using multi-dimensional metabolic profiling in ... ...

Abstract	Neuroblastoma (NB) is a childhood cancer arising from sympatho-adrenal neural crest cells. MYCN amplification is found in half of high-risk NB patients; however, no available therapies directly target MYCN. Using multi-dimensional metabolic profiling in MYCN expression systems and primary patient tumors, we comprehensively characterized the metabolic landscape driven by MYCN in NB. MYCN amplification leads to glycerolipid accumulation by promoting fatty acid (FA) uptake and biosynthesis. We found that cells expressing amplified MYCN depend highly on FA uptake for survival. Mechanistically, MYCN directly upregulates FA transport protein 2 (FATP2), encoded by SLC27A2. Genetic depletion of SLC27A2 impairs NB survival, and pharmacological SLC27A2 inhibition selectively suppresses tumor growth, prolongs animal survival, and exerts synergistic anti-tumor effects when combined with conventional chemotherapies in multiple preclinical NB models. This study identifies FA uptake as a critical metabolic dependency for MYCN-amplified tumors. Inhibiting FA uptake is an effective approach for improving current treatment regimens.
MeSH term(s)	Animals ; Cell Line, Tumor ; Fatty Acids ; N-Myc Proto-Oncogene Protein/genetics ; N-Myc Proto-Oncogene Protein/metabolism ; Neuroblastoma/metabolism
Chemical Substances	Fatty Acids ; N-Myc Proto-Oncogene Protein
Language	English
Publishing date	2022-06-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-31331-2
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Article ; Online: MYCN-driven fatty acid uptake is a metabolic vulnerability in neuroblastoma

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 17

Abstract: Half of high-risk neuroblastoma patients have MYCN amplification. Here, the authors show that MYCN induces fatty acid uptake and synthesis to support neuroblastoma and inhibition of a fatty acid transporter impairs tumor progression in preclinical models. ...

Abstract	Half of high-risk neuroblastoma patients have MYCN amplification. Here, the authors show that MYCN induces fatty acid uptake and synthesis to support neuroblastoma and inhibition of a fatty acid transporter impairs tumor progression in preclinical models.
Keywords	Science ; Q
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Restoration of the molecular clock is tumor suppressive in neuroblastoma.

Moreno-Smith, Myrthala / Milazzo, Giorgio / Tao, Ling / Fekry, Baharan / Zhu, Bokai / Mohammad, Mahmoud A / Di Giacomo, Simone / Borkar, Roshan / Reddy, Karthik Reddy Kami / Capasso, Mario / Vasudevan, Sanjeev A / Sumazin, Pavel / Hicks, John / Putluri, Nagireddy / Perini, Giovanni / Eckel-Mahan, Kristin / Burris, Thomas P / Barbieri, Eveline

Nature communications

2021 Volume 12, Issue 1, Page(s) 4006

Abstract: MYCN activation is a hallmark of advanced neuroblastoma (NB) and a known master regulator of metabolic reprogramming, favoring NB adaptation to its microenvironment. We found that the expression of the main regulators of the molecular clock loops is ... ...

Abstract	MYCN activation is a hallmark of advanced neuroblastoma (NB) and a known master regulator of metabolic reprogramming, favoring NB adaptation to its microenvironment. We found that the expression of the main regulators of the molecular clock loops is profoundly disrupted in MYCN-amplified NB patients, and this disruption independently predicts poor clinical outcome. MYCN induces the expression of clock repressors and downregulates the one of clock activators by directly binding to their promoters. Ultimately, MYCN attenuates the molecular clock by suppressing BMAL1 expression and oscillation, thereby promoting cell survival. Reestablishment of the activity of the clock activator RORα via its genetic overexpression and its stimulation through the agonist SR1078, restores BMAL1 expression and oscillation, effectively blocks MYCN-mediated tumor growth and de novo lipogenesis, and sensitizes NB tumors to conventional chemotherapy. In conclusion, reactivation of RORα could serve as a therapeutic strategy for MYCN-amplified NBs by blocking the dysregulation of molecular clock and cell metabolism mediated by MYCN.
MeSH term(s)	ARNTL Transcription Factors/metabolism ; Animals ; Antineoplastic Agents/therapeutic use ; Benzamides/pharmacology ; Cell Line, Tumor ; Cell Survival/physiology ; Humans ; Lipogenesis/physiology ; Mice ; N-Myc Proto-Oncogene Protein/metabolism ; Neuroblastoma/drug therapy ; Neuroblastoma/pathology ; Nuclear Receptor Subfamily 1, Group F, Member 1/metabolism ; Promoter Regions, Genetic/genetics ; Xenograft Model Antitumor Assays
Chemical Substances	ARNTL Transcription Factors ; BMAL1 protein, human ; Antineoplastic Agents ; Benzamides ; MYCN protein, human ; N-Myc Proto-Oncogene Protein ; Nuclear Receptor Subfamily 1, Group F, Member 1 ; RORA protein, human ; SR 1078
Language	English
Publishing date	2021-06-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-24196-4
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Article ; Online: The synergy of BET inhibitors with aurora A kinase inhibitors in MYCN-amplified neuroblastoma is heightened with functional TP53.

Yi, Joanna S / Sias-Garcia, Oscar / Nasholm, Nicole / Hu, Xiaoyu / Iniguez, Amanda Balboni / Hall, Matthew D / Davis, Mindy / Guha, Rajarshi / Moreno-Smith, Myrthala / Barbieri, Eveline / Duong, Kevin / Koach, Jessica / Qi, Jun / Bradner, James E / Stegmaier, Kimberly / Weiss, William A / Gustafson, W Clay

Neoplasia (New York, N.Y.)

2021 Volume 23, Issue 6, Page(s) 624–633

Abstract: Amplification of MYCN is a poor prognostic feature in neuroblastoma (NBL) indicating aggressive disease. We and others have shown BET bromodomain inhibitors (BETi) target MYCN indirectly by downregulating its transcription. Here we sought to identify ... ...

Abstract	Amplification of MYCN is a poor prognostic feature in neuroblastoma (NBL) indicating aggressive disease. We and others have shown BET bromodomain inhibitors (BETi) target MYCN indirectly by downregulating its transcription. Here we sought to identify agents that synergize with BETi and to identify biomarkers of resistance. We previously performed a viability screen of ∼1,900 oncology-focused compounds combined with BET bromodomain inhibitors against MYCN-amplified NBL cell lines. Reanalysis of our screening results prominently identified inhibitors of aurora kinase A (AURKAi) to be highly synergistic with BETi. We confirmed the anti-proliferative effects of several BETi+AURKAi combinations in MYCN-amplified NBL cell lines. Compared to single agents, these combinations cooperated to decrease levels of N-myc. We treated both TP53-wild type and mutant, MYCN-amplified cell lines with the BETi JQ1 and the AURKAi Alisertib. The combination had improved efficacy in the TP53-WT context, notably driving apoptosis in both genetic backgrounds. JQ1+Alisertib combination treatment of a MYCN-amplified, TP53-null or TP53-restored genetically engineered mouse model of NBL prolonged survival better than either single agent. This was most profound with TP53 restored, with marked tumor shrinkage and apoptosis induction in response to combination JQ1+Alisertib. BETi+AURKAi in MYCN-amplified NBL, particularly in the context of functional TP53, provided anti-tumor benefits in preclinical models. This combination should be studied more closely in a pediatric clinical trial.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; Aurora Kinase A/antagonists & inhibitors ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival ; Gene Amplification ; Gene Editing ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Immunohistochemistry ; Mice ; N-Myc Proto-Oncogene Protein/antagonists & inhibitors ; N-Myc Proto-Oncogene Protein/genetics ; N-Myc Proto-Oncogene Protein/metabolism ; Neuroblastoma/drug therapy ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Neuroblastoma/pathology ; Protein Kinase Inhibitors/pharmacology ; Proteins/antagonists & inhibitors ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	MYCN protein, human ; N-Myc Proto-Oncogene Protein ; Protein Kinase Inhibitors ; Proteins ; Tumor Suppressor Protein p53 ; bromodomain and extra-terminal domain protein, human ; Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2021-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2021.05.003
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Article ; Online: CHAF1A Blocks Neuronal Differentiation and Promotes Neuroblastoma Oncogenesis via Metabolic Reprogramming.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2021 Volume 8, Issue 19, Page(s) e2005047

Abstract: Neuroblastoma (NB) arises from oncogenic disruption of neural crest (NC) differentiation. Treatment with retinoic acid (RA) to induce differentiation has improved survival in some NB patients, but not all patients respond, and most NBs eventually develop ...

Abstract	Neuroblastoma (NB) arises from oncogenic disruption of neural crest (NC) differentiation. Treatment with retinoic acid (RA) to induce differentiation has improved survival in some NB patients, but not all patients respond, and most NBs eventually develop resistance to RA. Loss of the chromatin modifier chromatin assembly factor 1 subunit p150 (CHAF1A) promotes NB cell differentiation; however, the mechanism by which CHAF1A drives NB oncogenesis has remained unexplored. This study shows that CHAF1A gain-of-function supports cell malignancy, blocks neuronal differentiation in three models (zebrafish NC, human NC, and human NB), and promotes NB oncogenesis. Mechanistically, CHAF1A upregulates polyamine metabolism, which blocks neuronal differentiation and promotes cell cycle progression. Targeting polyamine synthesis promotes NB differentiation and enhances the anti-tumor activity of RA. The authors' results provide insight into the mechanisms that drive NB oncogenesis and suggest a rapidly translatable therapeutic approach (DFMO plus RA) to enhance the clinical efficacy of differentiation therapy in NB patients.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Cell Differentiation/genetics ; Cell Line, Tumor ; Chromatin Assembly Factor-1/genetics ; Chromatin Assembly Factor-1/metabolism ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Male ; Mice ; Mice, Nude ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Neurons/metabolism ; Zebrafish
Chemical Substances	CHAF1A protein, human ; Chaf1a protein, mouse ; Chromatin Assembly Factor-1
Language	English
Publishing date	2021-08-08
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202005047
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Article ; Online: Restoration of the molecular clock is tumor suppressive in neuroblastoma

Myrthala Moreno-Smith / Giorgio Milazzo / Ling Tao / Baharan Fekry / Bokai Zhu / Mahmoud A. Mohammad / Simone Di Giacomo / Roshan Borkar / Karthik Reddy Kami Reddy / Mario Capasso / Sanjeev A. Vasudevan / Pavel Sumazin / John Hicks / Nagireddy Putluri / Giovanni Perini / Kristin Eckel-Mahan / Thomas P. Burris / Eveline Barbieri

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 16

Abstract: MYCN is frequently amplified in neuroblastomas. Here, the authors show that MYCN disrupts the molecular clock by downregulating clock activator RORα and that the reactivation of RORα restores BMAL1 activity, and inhibits lipid metabolism and ... ...

Abstract	MYCN is frequently amplified in neuroblastomas. Here, the authors show that MYCN disrupts the molecular clock by downregulating clock activator RORα and that the reactivation of RORα restores BMAL1 activity, and inhibits lipid metabolism and neuroblastoma growth
Keywords	Science ; Q
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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