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Identification of flubendazole as potential anti-neuroblastoma compound in a large cell line screen

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Identification of flubendazole as potential anti-neuroblastoma compound in a large cell line screen. / Michaelis, Martin; Agha, Bishr; Rothweiler, Florian; Löschmann, Nadine; Voges, Yvonne; Mittelbronn, Michel; Starzetz, Tatjana; Harter, Patrick N; Abhari, Behnaz A; Fulda, Simone; Westermann, Frank; Riecken, Kristoffer; Spek, Silvia; Langer, Klaus; Wiese, Michael; Dirks, Wilhelm G; Zehner, Richard; Cinatl, Jaroslav; Wass, Mark N; Cinatl, Jindrich.

in: SCI REP-UK, Jahrgang 5, 01.01.2015, S. 8202.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Michaelis, M, Agha, B, Rothweiler, F, Löschmann, N, Voges, Y, Mittelbronn, M, Starzetz, T, Harter, PN, Abhari, BA, Fulda, S, Westermann, F, Riecken, K, Spek, S, Langer, K, Wiese, M, Dirks, WG, Zehner, R, Cinatl, J, Wass, MN & Cinatl, J 2015, 'Identification of flubendazole as potential anti-neuroblastoma compound in a large cell line screen', SCI REP-UK, Jg. 5, S. 8202. https://doi.org/10.1038/srep08202

APA

Michaelis, M., Agha, B., Rothweiler, F., Löschmann, N., Voges, Y., Mittelbronn, M., Starzetz, T., Harter, P. N., Abhari, B. A., Fulda, S., Westermann, F., Riecken, K., Spek, S., Langer, K., Wiese, M., Dirks, W. G., Zehner, R., Cinatl, J., Wass, M. N., & Cinatl, J. (2015). Identification of flubendazole as potential anti-neuroblastoma compound in a large cell line screen. SCI REP-UK, 5, 8202. https://doi.org/10.1038/srep08202

Vancouver

Michaelis M, Agha B, Rothweiler F, Löschmann N, Voges Y, Mittelbronn M et al. Identification of flubendazole as potential anti-neuroblastoma compound in a large cell line screen. SCI REP-UK. 2015 Jan 1;5:8202. https://doi.org/10.1038/srep08202

Bibtex

@article{706f6879949b41bbaa1c1170b92b74d4,
title = "Identification of flubendazole as potential anti-neuroblastoma compound in a large cell line screen",
abstract = "Flubendazole was shown to exert anti-leukaemia and anti-myeloma activity through inhibition of microtubule function. Here, flubendazole was tested for its effects on the viability of in total 461 cancer cell lines. Neuroblastoma was identified as highly flubendazole-sensitive cancer entity in a screen of 321 cell lines from 26 cancer entities. Flubendazole also reduced the viability of five primary neuroblastoma samples in nanomolar concentrations thought to be achievable in humans and inhibited vessel formation and neuroblastoma tumour growth in the chick chorioallantoic membrane assay. Resistance acquisition is a major problem in high-risk neuroblastoma. 119 cell lines from a panel of 140 neuroblastoma cell lines with acquired resistance to various anti-cancer drugs were sensitive to flubendazole in nanomolar concentrations. Tubulin-binding agent-resistant cell lines displayed the highest flubendazole IC50 and IC90 values but differences between drug classes did not reach statistical significance. Flubendazole induced p53-mediated apoptosis. The siRNA-mediated depletion of the p53 targets p21, BAX, or PUMA reduced the neuroblastoma cell sensitivity to flubendazole with PUMA depletion resulting in the most pronounced effects. The MDM2 inhibitor and p53 activator nutlin-3 increased flubendazole efficacy while RNAi-mediated p53-depletion reduced its activity. In conclusion, flubendazole represents a potential treatment option for neuroblastoma including therapy-refractory cells.",
author = "Martin Michaelis and Bishr Agha and Florian Rothweiler and Nadine L{\"o}schmann and Yvonne Voges and Michel Mittelbronn and Tatjana Starzetz and Harter, {Patrick N} and Abhari, {Behnaz A} and Simone Fulda and Frank Westermann and Kristoffer Riecken and Silvia Spek and Klaus Langer and Michael Wiese and Dirks, {Wilhelm G} and Richard Zehner and Jaroslav Cinatl and Wass, {Mark N} and Jindrich Cinatl",
year = "2015",
month = jan,
day = "1",
doi = "10.1038/srep08202",
language = "English",
volume = "5",
pages = "8202",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Identification of flubendazole as potential anti-neuroblastoma compound in a large cell line screen

AU - Michaelis, Martin

AU - Agha, Bishr

AU - Rothweiler, Florian

AU - Löschmann, Nadine

AU - Voges, Yvonne

AU - Mittelbronn, Michel

AU - Starzetz, Tatjana

AU - Harter, Patrick N

AU - Abhari, Behnaz A

AU - Fulda, Simone

AU - Westermann, Frank

AU - Riecken, Kristoffer

AU - Spek, Silvia

AU - Langer, Klaus

AU - Wiese, Michael

AU - Dirks, Wilhelm G

AU - Zehner, Richard

AU - Cinatl, Jaroslav

AU - Wass, Mark N

AU - Cinatl, Jindrich

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Flubendazole was shown to exert anti-leukaemia and anti-myeloma activity through inhibition of microtubule function. Here, flubendazole was tested for its effects on the viability of in total 461 cancer cell lines. Neuroblastoma was identified as highly flubendazole-sensitive cancer entity in a screen of 321 cell lines from 26 cancer entities. Flubendazole also reduced the viability of five primary neuroblastoma samples in nanomolar concentrations thought to be achievable in humans and inhibited vessel formation and neuroblastoma tumour growth in the chick chorioallantoic membrane assay. Resistance acquisition is a major problem in high-risk neuroblastoma. 119 cell lines from a panel of 140 neuroblastoma cell lines with acquired resistance to various anti-cancer drugs were sensitive to flubendazole in nanomolar concentrations. Tubulin-binding agent-resistant cell lines displayed the highest flubendazole IC50 and IC90 values but differences between drug classes did not reach statistical significance. Flubendazole induced p53-mediated apoptosis. The siRNA-mediated depletion of the p53 targets p21, BAX, or PUMA reduced the neuroblastoma cell sensitivity to flubendazole with PUMA depletion resulting in the most pronounced effects. The MDM2 inhibitor and p53 activator nutlin-3 increased flubendazole efficacy while RNAi-mediated p53-depletion reduced its activity. In conclusion, flubendazole represents a potential treatment option for neuroblastoma including therapy-refractory cells.

AB - Flubendazole was shown to exert anti-leukaemia and anti-myeloma activity through inhibition of microtubule function. Here, flubendazole was tested for its effects on the viability of in total 461 cancer cell lines. Neuroblastoma was identified as highly flubendazole-sensitive cancer entity in a screen of 321 cell lines from 26 cancer entities. Flubendazole also reduced the viability of five primary neuroblastoma samples in nanomolar concentrations thought to be achievable in humans and inhibited vessel formation and neuroblastoma tumour growth in the chick chorioallantoic membrane assay. Resistance acquisition is a major problem in high-risk neuroblastoma. 119 cell lines from a panel of 140 neuroblastoma cell lines with acquired resistance to various anti-cancer drugs were sensitive to flubendazole in nanomolar concentrations. Tubulin-binding agent-resistant cell lines displayed the highest flubendazole IC50 and IC90 values but differences between drug classes did not reach statistical significance. Flubendazole induced p53-mediated apoptosis. The siRNA-mediated depletion of the p53 targets p21, BAX, or PUMA reduced the neuroblastoma cell sensitivity to flubendazole with PUMA depletion resulting in the most pronounced effects. The MDM2 inhibitor and p53 activator nutlin-3 increased flubendazole efficacy while RNAi-mediated p53-depletion reduced its activity. In conclusion, flubendazole represents a potential treatment option for neuroblastoma including therapy-refractory cells.

U2 - 10.1038/srep08202

DO - 10.1038/srep08202

M3 - SCORING: Journal article

C2 - 25644037

VL - 5

SP - 8202

JO - SCI REP-UK

JF - SCI REP-UK

SN - 2045-2322

ER -