Home > Research > Publications & Outputs > An ILK/STAT3 pathway controls glioblastoma stem...

Research

Links

Text available via DOI:

View graph of relations

An ILK/STAT3 pathway controls glioblastoma stem cell plasticity

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Published

Standard

An ILK/STAT3 pathway controls glioblastoma stem cell plasticity. / Loftus, Alexander E P; Romano, Marianna S; Phuong, Anh Nguyen et al.
In: Developmental Cell, Vol. 59, No. 24, 16.12.2024, p. 3197-3212.e7.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Loftus, AEP, Romano, MS, Phuong, AN, McKinnel, BJ, Muir, MT, Furqan, M, Dawson, JC, Avalle, L, Douglas, AT, Mort, RL, Byron, A, Carragher, NO, Pollard, SM, Brunton, VG & Frame, MC 2024, 'An ILK/STAT3 pathway controls glioblastoma stem cell plasticity', Developmental Cell, vol. 59, no. 24, pp. 3197-3212.e7. https://doi.org/10.1016/j.devcel.2024.09.003

APA

Loftus, A. E. P., Romano, M. S., Phuong, A. N., McKinnel, B. J., Muir, M. T., Furqan, M., Dawson, J. C., Avalle, L., Douglas, A. T., Mort, R. L., Byron, A., Carragher, N. O., Pollard, S. M., Brunton, V. G., & Frame, M. C. (2024). An ILK/STAT3 pathway controls glioblastoma stem cell plasticity. Developmental Cell, 59(24), 3197-3212.e7. https://doi.org/10.1016/j.devcel.2024.09.003

Vancouver

Loftus AEP, Romano MS, Phuong AN, McKinnel BJ, Muir MT, Furqan M et al. An ILK/STAT3 pathway controls glioblastoma stem cell plasticity. Developmental Cell. 2024 Dec 16;59(24):3197-3212.e7. doi: 10.1016/j.devcel.2024.09.003

Author

Loftus, Alexander E P ; Romano, Marianna S ; Phuong, Anh Nguyen et al. / An ILK/STAT3 pathway controls glioblastoma stem cell plasticity. In: Developmental Cell. 2024 ; Vol. 59, No. 24. pp. 3197-3212.e7.

Bibtex

@article{6bdfbac144ad45eeb184e1c23d6d246a,
title = "An ILK/STAT3 pathway controls glioblastoma stem cell plasticity",
abstract = "Glioblastoma (GBM) is driven by malignant neural stem-like cells that display extensive heterogeneity and phenotypic plasticity, which drive tumor progression and therapeutic resistance. Here, we show that the extracellular matrix-cell adhesion protein integrin-linked kinase (ILK) stimulates phenotypic plasticity and mesenchymal-like, invasive behavior in a murine GBM stem cell model. ILK is required for the interconversion of GBM stem cells between malignancy-associated glial-like states, and its loss produces cells that are unresponsive to multiple cell state transition cues. We further show that an ILK/STAT3 signaling pathway controls the plasticity that enables transition of GBM stem cells to an astrocyte-like state in vitro and in vivo. Finally, we find that ILK expression correlates with expression of STAT3-regulated proteins and protein signatures describing astrocyte-like and mesenchymal states in patient tumors. This work identifies ILK as a pivotal regulator of multiple malignancy-associated GBM phenotypes, including phenotypic plasticity and mesenchymal state.",
author = "Loftus, {Alexander E P} and Romano, {Marianna S} and Phuong, {Anh Nguyen} and McKinnel, {Ben J} and Muir, {Morwenna T} and Muhammad Furqan and Dawson, {John C} and Lidia Avalle and Douglas, {Adam T} and Mort, {Richard L} and Adam Byron and Carragher, {Neil O} and Pollard, {Steven M} and Brunton, {Valerie G} and Frame, {Margaret C}",
note = "Copyright {\textcopyright} 2024 The Author(s). Published by Elsevier Inc. All rights reserved.",
year = "2024",
month = dec,
day = "16",
doi = "10.1016/j.devcel.2024.09.003",
language = "English",
volume = "59",
pages = "3197--3212.e7",
journal = "Developmental Cell",
issn = "1534-5807",
publisher = "Cell Press",
number = "24",

}

RIS

TY - JOUR

T1 - An ILK/STAT3 pathway controls glioblastoma stem cell plasticity

AU - Loftus, Alexander E P

AU - Romano, Marianna S

AU - Phuong, Anh Nguyen

AU - McKinnel, Ben J

AU - Muir, Morwenna T

AU - Furqan, Muhammad

AU - Dawson, John C

AU - Avalle, Lidia

AU - Douglas, Adam T

AU - Mort, Richard L

AU - Byron, Adam

AU - Carragher, Neil O

AU - Pollard, Steven M

AU - Brunton, Valerie G

AU - Frame, Margaret C

N1 - Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

PY - 2024/12/16

Y1 - 2024/12/16

N2 - Glioblastoma (GBM) is driven by malignant neural stem-like cells that display extensive heterogeneity and phenotypic plasticity, which drive tumor progression and therapeutic resistance. Here, we show that the extracellular matrix-cell adhesion protein integrin-linked kinase (ILK) stimulates phenotypic plasticity and mesenchymal-like, invasive behavior in a murine GBM stem cell model. ILK is required for the interconversion of GBM stem cells between malignancy-associated glial-like states, and its loss produces cells that are unresponsive to multiple cell state transition cues. We further show that an ILK/STAT3 signaling pathway controls the plasticity that enables transition of GBM stem cells to an astrocyte-like state in vitro and in vivo. Finally, we find that ILK expression correlates with expression of STAT3-regulated proteins and protein signatures describing astrocyte-like and mesenchymal states in patient tumors. This work identifies ILK as a pivotal regulator of multiple malignancy-associated GBM phenotypes, including phenotypic plasticity and mesenchymal state.

AB - Glioblastoma (GBM) is driven by malignant neural stem-like cells that display extensive heterogeneity and phenotypic plasticity, which drive tumor progression and therapeutic resistance. Here, we show that the extracellular matrix-cell adhesion protein integrin-linked kinase (ILK) stimulates phenotypic plasticity and mesenchymal-like, invasive behavior in a murine GBM stem cell model. ILK is required for the interconversion of GBM stem cells between malignancy-associated glial-like states, and its loss produces cells that are unresponsive to multiple cell state transition cues. We further show that an ILK/STAT3 signaling pathway controls the plasticity that enables transition of GBM stem cells to an astrocyte-like state in vitro and in vivo. Finally, we find that ILK expression correlates with expression of STAT3-regulated proteins and protein signatures describing astrocyte-like and mesenchymal states in patient tumors. This work identifies ILK as a pivotal regulator of multiple malignancy-associated GBM phenotypes, including phenotypic plasticity and mesenchymal state.

U2 - 10.1016/j.devcel.2024.09.003

DO - 10.1016/j.devcel.2024.09.003

M3 - Journal article

C2 - 39326421

VL - 59

SP - 3197-3212.e7

JO - Developmental Cell

JF - Developmental Cell

SN - 1534-5807

IS - 24

ER -