Underlying Mechanisms of Brain Cancer Spreading

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuro-oncology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 1888

Special Issue Editors


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Guest Editor
Department of Neurosurgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
Interests: brain cancer

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Guest Editor Assistant
Department of Neurosurgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
Interests: brain tumors

E-Mail Website
Guest Editor Assistant
Department of Neurosurgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
Interests: brain tumors

Special Issue Information

Dear Colleagues,

Dissemination of tumor cells from the primary tumor causes healthy tissue infiltration and metastatic disease, and it hampers the efficacy of current cancer treatments. It is triggered by the transient or permanent induction of motility and invasiveness in the tumor cells. An essential prerequisite for primary brain tumor cell migration and invasion is the remodeling of the actin and tubulin cytoskeletons, which not only provide force, traction and rigidity but also scaffold signaling complexes in a spatially controlled manner. Hence, blocking motility and invasiveness by targeting pro-migratory cytoskeleton dynamics in tumor cells could prevent local tumor cell invasion, further dissemination from proximal metastases and the evolution towards a more aggressive phenotype.

In this special issue we soliciting manuscripts that focus on the molecular, genetic and cellular mechanisms of brain cancer spreading.

Dr. Alireza Khoshnevisan
Guest Editor

Dr. Milad Shafizadeh
Dr. Samuel Kankam
Guest Editor Assistants

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Keywords

  • brain tumors
  • spreading
  • cancer

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Published Papers (1 paper)

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Research

13 pages, 2135 KiB  
Article
Interleukin-11/IL-11 Receptor Promotes Glioblastoma Cell Proliferation, Epithelial–Mesenchymal Transition, and Invasion
by Sarah F. Stuart, Peter Curpen, Adele J. Gomes, Michelle C. Lan, Shuai Nie, Nicholas A. Williamson, George Kannourakis, Andrew P. Morokoff, Adrian A. Achuthan and Rodney B. Luwor
Brain Sci. 2024, 14(1), 89; https://doi.org/10.3390/brainsci14010089 - 17 Jan 2024
Viewed by 1675
Abstract
Glioblastoma is highly proliferative and invasive. However, the regulatory cytokine networks that promote glioblastoma cell proliferation and invasion into other areas of the brain are not fully defined. In the present study, we define a critical role for the IL-11/IL-11Rα signalling axis in [...] Read more.
Glioblastoma is highly proliferative and invasive. However, the regulatory cytokine networks that promote glioblastoma cell proliferation and invasion into other areas of the brain are not fully defined. In the present study, we define a critical role for the IL-11/IL-11Rα signalling axis in glioblastoma proliferation, epithelial to mesenchymal transition, and invasion. We identified enhanced IL-11/IL-11Rα expression correlated with reduced overall survival in glioblastoma patients using TCGA datasets. Proteomic analysis of glioblastoma cell lines overexpressing IL-11Rα displayed a proteome that favoured enhanced proliferation and invasion. These cells also displayed greater proliferation and migration, while the knockdown of IL-11Rα reversed these tumourigenic characteristics. In addition, these IL-11Rα overexpressing cells displayed enhanced invasion in transwell invasion assays and in 3D spheroid invasion assays, while knockdown of IL-11Rα resulted in reduced invasion. Furthermore, IL-11Rα-overexpressing cells displayed a more mesenchymal-like phenotype compared to parental cells and expressed greater levels of the mesenchymal marker Vimentin. Overall, our study identified that the IL-11/IL-11Rα pathway promotes glioblastoma cell proliferation, EMT, and invasion. Full article
(This article belongs to the Special Issue Underlying Mechanisms of Brain Cancer Spreading)
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