Autophagy induction impairs Wnt/β-catenin signalling through β-catenin relocalisation in glioblastoma cells

Barbara Colella, Fiorella Faienza, Marianna Carinci, Giuseppina D'Alessandro, Myriam Catalano, Antonio Santoro, Francesco Cecconi, Cristina Limatola, Sabrina Di Bartolomeo

Research output: Contribution to journalArticle

Abstract

Autophagy is an evolutionary conserved process mediating lysosomal degradation of cytoplasmic material. Its involvement in cancer progression is highly controversial, due to its dual role in both limiting tumoural transformation and in protecting established tumoral cells from unfavorable conditions. Little is known about the cross-talk between autophagy and intracellular signalling pathways, as well as about autophagy impact on signalling molecules turnover. An aberrantly activated Wnt/β-catenin signalling is responsible for tumour proliferation, invasion, and stemness maintenance. Here we show that autophagy negatively regulates Wnt/β-catenin signalling in glioblastoma multiforme (GBM) cells, through Dishevelled degradation. We also provide the first evidence that autophagy promotes β-catenin relocalisation within the cell, by inducing a decrease of the nuclear protein fraction. In particular, upon autophagy induction, β-catenin appears mainly localized in sub-membrane areas where it associates with N-cadherin to form epithelial-like cell-cell adhesion structures. Our data indicate, for the first time, that autophagy induction results in Wnt signalling attenuation and in β-catenin relocalisation within the GBM cell. These findings further support the idea that autophagy modulation could represent a potential therapeutical strategy to contrast GBM progression.

Original languageEnglish
Pages (from-to)357-364
Number of pages8
JournalCellular Signalling
Volume53
DOIs
Publication statusPublished - Jan 2019

Fingerprint

Catenins
Autophagy
Glioblastoma
Cadherins
Nuclear Proteins
Cell Adhesion
Neoplasms
Epithelial Cells
Maintenance
Membranes

Cite this

Autophagy induction impairs Wnt/β-catenin signalling through β-catenin relocalisation in glioblastoma cells. / Colella, Barbara; Faienza, Fiorella; Carinci, Marianna; D'Alessandro, Giuseppina; Catalano, Myriam; Santoro, Antonio; Cecconi, Francesco; Limatola, Cristina; Di Bartolomeo, Sabrina.

In: Cellular Signalling, Vol. 53, 01.2019, p. 357-364.

Research output: Contribution to journalArticle

@article{a7478e60b3a046b6ad7cdfeb921a8acc,
title = "Autophagy induction impairs Wnt/β-catenin signalling through β-catenin relocalisation in glioblastoma cells",
abstract = "Autophagy is an evolutionary conserved process mediating lysosomal degradation of cytoplasmic material. Its involvement in cancer progression is highly controversial, due to its dual role in both limiting tumoural transformation and in protecting established tumoral cells from unfavorable conditions. Little is known about the cross-talk between autophagy and intracellular signalling pathways, as well as about autophagy impact on signalling molecules turnover. An aberrantly activated Wnt/β-catenin signalling is responsible for tumour proliferation, invasion, and stemness maintenance. Here we show that autophagy negatively regulates Wnt/β-catenin signalling in glioblastoma multiforme (GBM) cells, through Dishevelled degradation. We also provide the first evidence that autophagy promotes β-catenin relocalisation within the cell, by inducing a decrease of the nuclear protein fraction. In particular, upon autophagy induction, β-catenin appears mainly localized in sub-membrane areas where it associates with N-cadherin to form epithelial-like cell-cell adhesion structures. Our data indicate, for the first time, that autophagy induction results in Wnt signalling attenuation and in β-catenin relocalisation within the GBM cell. These findings further support the idea that autophagy modulation could represent a potential therapeutical strategy to contrast GBM progression.",
author = "Barbara Colella and Fiorella Faienza and Marianna Carinci and Giuseppina D'Alessandro and Myriam Catalano and Antonio Santoro and Francesco Cecconi and Cristina Limatola and {Di Bartolomeo}, Sabrina",
note = "Copyright {\circledC} 2018 Elsevier Inc. All rights reserved.",
year = "2019",
month = "1",
doi = "10.1016/j.cellsig.2018.10.017",
language = "English",
volume = "53",
pages = "357--364",
journal = "Cellular Signalling",
issn = "0898-6568",
publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - Autophagy induction impairs Wnt/β-catenin signalling through β-catenin relocalisation in glioblastoma cells

AU - Colella, Barbara

AU - Faienza, Fiorella

AU - Carinci, Marianna

AU - D'Alessandro, Giuseppina

AU - Catalano, Myriam

AU - Santoro, Antonio

AU - Cecconi, Francesco

AU - Limatola, Cristina

AU - Di Bartolomeo, Sabrina

N1 - Copyright © 2018 Elsevier Inc. All rights reserved.

PY - 2019/1

Y1 - 2019/1

N2 - Autophagy is an evolutionary conserved process mediating lysosomal degradation of cytoplasmic material. Its involvement in cancer progression is highly controversial, due to its dual role in both limiting tumoural transformation and in protecting established tumoral cells from unfavorable conditions. Little is known about the cross-talk between autophagy and intracellular signalling pathways, as well as about autophagy impact on signalling molecules turnover. An aberrantly activated Wnt/β-catenin signalling is responsible for tumour proliferation, invasion, and stemness maintenance. Here we show that autophagy negatively regulates Wnt/β-catenin signalling in glioblastoma multiforme (GBM) cells, through Dishevelled degradation. We also provide the first evidence that autophagy promotes β-catenin relocalisation within the cell, by inducing a decrease of the nuclear protein fraction. In particular, upon autophagy induction, β-catenin appears mainly localized in sub-membrane areas where it associates with N-cadherin to form epithelial-like cell-cell adhesion structures. Our data indicate, for the first time, that autophagy induction results in Wnt signalling attenuation and in β-catenin relocalisation within the GBM cell. These findings further support the idea that autophagy modulation could represent a potential therapeutical strategy to contrast GBM progression.

AB - Autophagy is an evolutionary conserved process mediating lysosomal degradation of cytoplasmic material. Its involvement in cancer progression is highly controversial, due to its dual role in both limiting tumoural transformation and in protecting established tumoral cells from unfavorable conditions. Little is known about the cross-talk between autophagy and intracellular signalling pathways, as well as about autophagy impact on signalling molecules turnover. An aberrantly activated Wnt/β-catenin signalling is responsible for tumour proliferation, invasion, and stemness maintenance. Here we show that autophagy negatively regulates Wnt/β-catenin signalling in glioblastoma multiforme (GBM) cells, through Dishevelled degradation. We also provide the first evidence that autophagy promotes β-catenin relocalisation within the cell, by inducing a decrease of the nuclear protein fraction. In particular, upon autophagy induction, β-catenin appears mainly localized in sub-membrane areas where it associates with N-cadherin to form epithelial-like cell-cell adhesion structures. Our data indicate, for the first time, that autophagy induction results in Wnt signalling attenuation and in β-catenin relocalisation within the GBM cell. These findings further support the idea that autophagy modulation could represent a potential therapeutical strategy to contrast GBM progression.

U2 - 10.1016/j.cellsig.2018.10.017

DO - 10.1016/j.cellsig.2018.10.017

M3 - Article

C2 - 30442596

VL - 53

SP - 357

EP - 364

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

ER -