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SKP2 Activation by Thyroid Hormone Receptor β2 Bypasses Rb-Dependent Proliferation in Rb-Deficient Cells

Sensitivity to germline RB1 mutations can be conferred by a cell type–restricted thyroid hormone receptor isoform that fulfills otherwise Rb-dependent cell-cycle and survival function. Germline RB1 mutations strongly predispose humans to cone precursor–derived retinoblastomas and strongly predispose... Full description

Journal Title: Cancer Research Dec 15, 2017, Vol.77(24), pp.6838-6850
Main Author: Xu, Xiaoliang
Other Authors: Liu, Aihong , Dan-Ning, Hu , Dong-Lai, Qi , Chitty, David , Wang, Justin , Zou, Jun , Weiss, Rebecca , Huang, Hongyan , Joseph, Walter , Ng, Lily , Rosen, Richard , Reid, Mark , Forrest, Douglas , Abramson, David , Singer, Samuel , Cobrinik, David , Jhanwar, Suresh
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 00085472 ; E-ISSN: 15387445 ; DOI: 10.1158/0008-5472.CAN-16-3299
Link: http://search.proquest.com/docview/1983250306/?pq-origsite=primo
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title: SKP2 Activation by Thyroid Hormone Receptor β2 Bypasses Rb-Dependent Proliferation in Rb-Deficient Cells
format: Article
creator:
  • Xu, Xiaoliang
  • Liu, Aihong
  • Dan-Ning, Hu
  • Dong-Lai, Qi
  • Chitty, David
  • Wang, Justin
  • Zou, Jun
  • Weiss, Rebecca
  • Huang, Hongyan
  • Joseph, Walter
  • Ng, Lily
  • Rosen, Richard
  • Reid, Mark
  • Forrest, Douglas
  • Abramson, David
  • Singer, Samuel
  • Cobrinik, David
  • Jhanwar, Suresh
subjects:
  • Brain Tumors
  • Pituitary
  • Tumors
  • Tumors
  • Thyroid
  • Viability
  • Neuroblastoma Cells
  • Cancer
  • Mutation
  • Skp2 Protein
  • Cell Proliferation
  • Ubiquitin-Protein Ligase
  • Tumorigenesis
  • Neuroblastoma
  • Thyroid Gland
  • Ubiquitin
  • Circuits
  • Thyroid
  • Tumors
  • Cancer
ispartof: Cancer Research, Dec 15, 2017, Vol.77(24), pp.6838-6850
description: Sensitivity to germline RB1 mutations can be conferred by a cell type–restricted thyroid hormone receptor isoform that fulfills otherwise Rb-dependent cell-cycle and survival function. Germline RB1 mutations strongly predispose humans to cone precursor–derived retinoblastomas and strongly predispose mice to pituitary tumors, yet shared cell type–specific circuitry that sensitizes these different cell types to the loss of RB1 has not been defined. Here we show that the cell type–restricted thyroid hormone receptor isoform TRβ2 sensitizes to RB1 loss in both settings by antagonizing the widely expressed and tumor-suppressive TRβ1. TRβ2 promoted expression of the E3 ubiquitin ligase SKP2, a critical factor for RB1-mutant tumors, by enabling EMI1/FBXO5–dependent inhibition of SKP2 degradation. In RB1 wild-type neuroblastoma cells, endogenous Rb or ectopic TRβ2 was required to sustain SKP2 expression as well as cell viability and proliferation. These results suggest that in certain contexts,...
language: eng
source:
identifier: ISSN: 00085472 ; E-ISSN: 15387445 ; DOI: 10.1158/0008-5472.CAN-16-3299
fulltext: fulltext
issn:
  • 00085472
  • 0008-5472
  • 15387445
  • 1538-7445
url: Link


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titleSKP2 Activation by Thyroid Hormone Receptor β2 Bypasses Rb-Dependent Proliferation in Rb-Deficient Cells
creatorXu, Xiaoliang ; Liu, Aihong ; Dan-Ning, Hu ; Dong-Lai, Qi ; Chitty, David ; Wang, Justin ; Zou, Jun ; Weiss, Rebecca ; Huang, Hongyan ; Joseph, Walter ; Ng, Lily ; Rosen, Richard ; Reid, Mark ; Forrest, Douglas ; Abramson, David ; Singer, Samuel ; Cobrinik, David ; Jhanwar, Suresh
ispartofCancer Research, Dec 15, 2017, Vol.77(24), pp.6838-6850
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subjectBrain Tumors ; Pituitary ; Tumors ; Tumors ; Thyroid ; Viability ; Neuroblastoma Cells ; Cancer ; Mutation ; Skp2 Protein ; Cell Proliferation ; Ubiquitin-Protein Ligase ; Tumorigenesis ; Neuroblastoma ; Thyroid Gland ; Ubiquitin ; Circuits ; Thyroid ; Tumors ; Cancer
descriptionSensitivity to germline RB1 mutations can be conferred by a cell type–restricted thyroid hormone receptor isoform that fulfills otherwise Rb-dependent cell-cycle and survival function. Germline RB1 mutations strongly predispose humans to cone precursor–derived retinoblastomas and strongly predispose mice to pituitary tumors, yet shared cell type–specific circuitry that sensitizes these different cell types to the loss of RB1 has not been defined. Here we show that the cell type–restricted thyroid hormone receptor isoform TRβ2 sensitizes to RB1 loss in both settings by antagonizing the widely expressed and tumor-suppressive TRβ1. TRβ2 promoted expression of the E3 ubiquitin ligase SKP2, a critical factor for RB1-mutant tumors, by enabling EMI1/FBXO5–dependent inhibition of SKP2 degradation. In RB1 wild-type neuroblastoma cells, endogenous Rb or ectopic TRβ2 was required to sustain SKP2 expression as well as cell viability and proliferation. These results suggest that in certain contexts,...
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titleSKP2 Activation by Thyroid Hormone Receptor β2 Bypasses Rb-Dependent Proliferation in Rb-Deficient Cells
descriptionSensitivity to germline RB1 mutations can be conferred by a cell type–restricted thyroid hormone receptor isoform that fulfills otherwise Rb-dependent cell-cycle and survival function. Germline RB1 mutations strongly predispose humans to cone precursor–derived retinoblastomas and strongly predispose mice to pituitary tumors, yet shared cell type–specific circuitry that sensitizes these different cell types to the loss of RB1 has not been defined. Here we show that the cell type–restricted thyroid hormone receptor isoform TRβ2 sensitizes to RB1 loss in both settings by antagonizing the widely expressed and tumor-suppressive TRβ1. TRβ2 promoted expression of the E3 ubiquitin ligase SKP2, a critical factor for RB1-mutant tumors, by enabling EMI1/FBXO5–dependent inhibition of SKP2 degradation. In RB1 wild-type neuroblastoma cells, endogenous Rb or ectopic TRβ2 was required to sustain SKP2 expression as well as cell viability and proliferation. These results suggest that in certain contexts,...
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titleSKP2 Activation by Thyroid Hormone Receptor β2 Bypasses Rb-Dependent Proliferation in Rb-Deficient Cells
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abstractSensitivity to germline RB1 mutations can be conferred by a cell type–restricted thyroid hormone receptor isoform that fulfills otherwise Rb-dependent cell-cycle and survival function. Germline RB1 mutations strongly predispose humans to cone precursor–derived retinoblastomas and strongly predispose mice to pituitary tumors, yet shared cell type–specific circuitry that sensitizes these different cell types to the loss of RB1 has not been defined. Here we show that the cell type–restricted thyroid hormone receptor isoform TRβ2 sensitizes to RB1 loss in both settings by antagonizing the widely expressed and tumor-suppressive TRβ1. TRβ2 promoted expression of the E3 ubiquitin ligase SKP2, a critical factor for RB1-mutant tumors, by enabling EMI1/FBXO5–dependent inhibition of SKP2 degradation. In RB1 wild-type neuroblastoma cells, endogenous Rb or ectopic TRβ2 was required to sustain SKP2 expression as well as cell viability and proliferation. These results suggest that in certain contexts,...
copBaltimore
pubAmerican Association for Cancer Research, Inc.
doi10.1158/0008-5472.CAN-16-3299
urlhttp://search.proquest.com/docview/1983250306/
date2017-12-15