PortalPublikationenDexamethasone destabilizes Nmyc to inhibit the growth of hed...

Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma

Standard

Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma. / Heine, Vivi M; Priller, Markus; Ling, Jason; Rowitch, David H; Schüller, Ulrich.

in: CANCER RES, Jahrgang 70, Nr. 13, 01.07.2010, S. 5220-5.

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

Harvard

Heine, VM, Priller, M, Ling, J, Rowitch, DH & Schüller, U 2010, 'Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma', CANCER RES, Jg. 70, Nr. 13, S. 5220-5. https://doi.org/10.1158/0008-5472.CAN-10-0554

APA

Heine, V. M., Priller, M., Ling, J., Rowitch, D. H., & Schüller, U. (2010). Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma. CANCER RES, 70(13), 5220-5. https://doi.org/10.1158/0008-5472.CAN-10-0554

Vancouver

Heine VM, Priller M, Ling J, Rowitch DH, Schüller U. Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma. CANCER RES. 2010 Jul 1;70(13):5220-5. https://doi.org/10.1158/0008-5472.CAN-10-0554

Bibtex

@article{9dca104726c64c87a35c30093c1ea20e,
title = "Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma",
abstract = "Mouse studies indicate that the synthetic glucocorticoid dexamethasone (Dex) impairs the proliferation of granule neuron precursors in the cerebellum, which are transformed to medulloblastoma by activation of Sonic hedgehog (Shh) signaling. Here, we show that Dex treatment also inhibits Shh-induced tumor growth, enhancing the survival of tumor-prone transgenic mice. We found that Nmyc was specifically required in granule cells for Shh-induced tumorigenesis and that Dex acted to reduce Nmyc protein levels. Moreover, we found that Dex-induced destabilization of Nmyc is mediated by activation of glycogen synthase kinase 3beta, which targets Nmyc for proteasomal degradation. Together, our findings show that Dex antagonizes Shh signaling downstream of Smoothened in medulloblastoma.",
keywords = "Animals, Brain Neoplasms, Dexamethasone, Glycogen Synthase Kinase 3, Glycogen Synthase Kinase 3 beta, Hedgehog Proteins, Medulloblastoma, Mice, Mice, Transgenic, Phosphorylation, Protein Structure, Tertiary, Proto-Oncogene Proteins c-myc, Signal Transduction, Tumor Cells, Cultured, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "Heine, {Vivi M} and Markus Priller and Jason Ling and Rowitch, {David H} and Ulrich Sch{\"u}ller",
note = "Copyright 2010 AACR.",
year = "2010",
month = jul,
day = "1",
doi = "10.1158/0008-5472.CAN-10-0554",
language = "English",
volume = "70",
pages = "5220--5",
journal = "CANCER RES",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "13",

}

RIS

TY - JOUR

T1 - Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma

AU - Heine, Vivi M

AU - Priller, Markus

AU - Ling, Jason

AU - Rowitch, David H

AU - Schüller, Ulrich

N1 - Copyright 2010 AACR.

PY - 2010/7/1

Y1 - 2010/7/1

N2 - Mouse studies indicate that the synthetic glucocorticoid dexamethasone (Dex) impairs the proliferation of granule neuron precursors in the cerebellum, which are transformed to medulloblastoma by activation of Sonic hedgehog (Shh) signaling. Here, we show that Dex treatment also inhibits Shh-induced tumor growth, enhancing the survival of tumor-prone transgenic mice. We found that Nmyc was specifically required in granule cells for Shh-induced tumorigenesis and that Dex acted to reduce Nmyc protein levels. Moreover, we found that Dex-induced destabilization of Nmyc is mediated by activation of glycogen synthase kinase 3beta, which targets Nmyc for proteasomal degradation. Together, our findings show that Dex antagonizes Shh signaling downstream of Smoothened in medulloblastoma.

AB - Mouse studies indicate that the synthetic glucocorticoid dexamethasone (Dex) impairs the proliferation of granule neuron precursors in the cerebellum, which are transformed to medulloblastoma by activation of Sonic hedgehog (Shh) signaling. Here, we show that Dex treatment also inhibits Shh-induced tumor growth, enhancing the survival of tumor-prone transgenic mice. We found that Nmyc was specifically required in granule cells for Shh-induced tumorigenesis and that Dex acted to reduce Nmyc protein levels. Moreover, we found that Dex-induced destabilization of Nmyc is mediated by activation of glycogen synthase kinase 3beta, which targets Nmyc for proteasomal degradation. Together, our findings show that Dex antagonizes Shh signaling downstream of Smoothened in medulloblastoma.

KW - Animals

KW - Brain Neoplasms

KW - Dexamethasone

KW - Glycogen Synthase Kinase 3

KW - Glycogen Synthase Kinase 3 beta

KW - Hedgehog Proteins

KW - Medulloblastoma

KW - Mice

KW - Mice, Transgenic

KW - Phosphorylation

KW - Protein Structure, Tertiary

KW - Proto-Oncogene Proteins c-myc

KW - Signal Transduction

KW - Tumor Cells, Cultured

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1158/0008-5472.CAN-10-0554

DO - 10.1158/0008-5472.CAN-10-0554

M3 - SCORING: Journal article

C2 - 20530674

VL - 70

SP - 5220

EP - 5225

JO - CANCER RES

JF - CANCER RES

SN - 0008-5472

IS - 13

ER -