Thumbnail Image
Item

Autocrine CXCL8-dependent invasiveness triggers modulation of actin cytoskeletal network and cell dynamics

Antonosante, A
; 
Brandolini, L
; 
d'Angelo, M
; 
Benedetti, E
; 
Castelli, V
; 
Maestro, MD
; 
Luzzi, S
; 
Giordano, A
; 
Cimini, A
; 
Allegretti, M
Citations
Altmetric:
Genre
Journal Article
Date
2020-01-27
Advisor
Committee member
Group
Department
Subject
glioblastoma
 chemokine
 CXCL8
 cytoskeleton
 cell migration
Permanent link to this record
http://hdl.handle.net/20.500.12613/4506
Collections
Faculty/Researcher Works
Show all metadata
Files
Thumbnail Image
Autocrine CXCL8-dependent invasiveness triggers modulation of actin cytoskeletal network and cell dynamics.pdf
Adobe PDF, 5.62 MB
Research Projects
Organizational Units
Journal Issue
DOI
10.18632/aging.102733
Abstract
Glioblastoma (GB) is the most representative form of primary malignant brain tumour. Several studies indicated a pleiotropic role of CXCL8 in cancer due to its ability to modulate the tumour microenvironment, growth and aggressiveness of tumour cell. Previous studies indicated that CXCL8 by its receptors (CXCR1 and CXCR2) induced activation of the PI3K/p-Akt pathway, a crucial event in the regulation of cytoskeleton rearrangement and cell mobilization. Human GB primary cell culture and U-87MG cell line were used to study the effects of CXCR1 and CXCR2 blockage, by a dual allosteric antagonist, on cell migration and cytoskeletal dynamics. The data obtained point towards a specific effect of autocrine CXCL8 signalling on GB cell invasiveness by the activation of pathways involved in cell migration and cytoskeletal dynamics, such as PI3K/p-Akt/p-FAK, p-cortactin, RhoA, Cdc42, Acetylated α-tubulin and MMP2. All the data obtained support the concept that autocrine CXCL8 signalling plays a key role in the activation of an aggressive phenotype in primary glioblastoma cells and U-87MG cell line. These results provide new insights about the potential of a pharmacological approach targeting CXCR1/CXCR2 pathways to decrease migration and invasion of GB cells in the brain parenchyma, one of the principal mechanisms of recurrence.
Description
Citation
Citation to related work
Impact Journals, LLC
Has part
Aging
ADA compliance
For Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
Embedded videos