Cargando…

Polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro

The mechanobiological aspects of glioblastoma (GBM) pathogenesis are largely unknown. Polycystin‐1 (PC1) is a key mechanosensitive protein which perceives extracellular mechanical cues and transforms them into intracellular biochemical signals that elicit a change in cell behaviour. The aim of the p...

Descripción completa

Detalles Bibliográficos
Autores principales: Zoi, Ilianna, Gargalionis, Antonios N., Papavassiliou, Kostas A., Nasiri‐Ansari, Narjes, Piperi, Christina, Basdra, Efthimia K., Papavassiliou, Athanasios G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8899169/
https://www.ncbi.nlm.nih.gov/pubmed/35106909
http://dx.doi.org/10.1111/jcmm.17212
_version_ 1784663853862223872
author Zoi, Ilianna
Gargalionis, Antonios N.
Papavassiliou, Kostas A.
Nasiri‐Ansari, Narjes
Piperi, Christina
Basdra, Efthimia K.
Papavassiliou, Athanasios G.
author_facet Zoi, Ilianna
Gargalionis, Antonios N.
Papavassiliou, Kostas A.
Nasiri‐Ansari, Narjes
Piperi, Christina
Basdra, Efthimia K.
Papavassiliou, Athanasios G.
author_sort Zoi, Ilianna
collection PubMed
description The mechanobiological aspects of glioblastoma (GBM) pathogenesis are largely unknown. Polycystin‐1 (PC1) is a key mechanosensitive protein which perceives extracellular mechanical cues and transforms them into intracellular biochemical signals that elicit a change in cell behaviour. The aim of the present study was to investigate if and how PC1 participates in GBM pathogenesis under a mechanically induced microenvironment. Therefore, we subjected T98G GBM cells to continuous hydrostatic pressure (HP) and/or PC1 blockade and evaluated their effect on cell behaviour, the activity of signalling pathways and the expression of mechano‐induced transcriptional regulators and markers associated with properties of cancer cells. According to our data, PC1 and HP affect GBM cell proliferation, clonogenicity and migration; the diameter of GBM spheroids; the phosphorylation of mechanistic target of rapamycin (mTOR), extracellular signal‐regulated kinase (ERK) and focal adhesion kinase (FAK); the protein expression of transcription cofactors YES‐associated protein (YAP) and transcriptional coactivator with PDZ‐binding motif (TAZ); and the mRNA expression of markers related to anti‐apoptosis, apoptosis, angiogenesis, epithelial to mesenchymal transition (EMT) and proliferation. Together, our in vitro results suggest that PC1 plays an important role in GBM mechanobiology.
format Online
Article
Text
id pubmed-8899169
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-88991692022-03-11 Polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro Zoi, Ilianna Gargalionis, Antonios N. Papavassiliou, Kostas A. Nasiri‐Ansari, Narjes Piperi, Christina Basdra, Efthimia K. Papavassiliou, Athanasios G. J Cell Mol Med Original Articles The mechanobiological aspects of glioblastoma (GBM) pathogenesis are largely unknown. Polycystin‐1 (PC1) is a key mechanosensitive protein which perceives extracellular mechanical cues and transforms them into intracellular biochemical signals that elicit a change in cell behaviour. The aim of the present study was to investigate if and how PC1 participates in GBM pathogenesis under a mechanically induced microenvironment. Therefore, we subjected T98G GBM cells to continuous hydrostatic pressure (HP) and/or PC1 blockade and evaluated their effect on cell behaviour, the activity of signalling pathways and the expression of mechano‐induced transcriptional regulators and markers associated with properties of cancer cells. According to our data, PC1 and HP affect GBM cell proliferation, clonogenicity and migration; the diameter of GBM spheroids; the phosphorylation of mechanistic target of rapamycin (mTOR), extracellular signal‐regulated kinase (ERK) and focal adhesion kinase (FAK); the protein expression of transcription cofactors YES‐associated protein (YAP) and transcriptional coactivator with PDZ‐binding motif (TAZ); and the mRNA expression of markers related to anti‐apoptosis, apoptosis, angiogenesis, epithelial to mesenchymal transition (EMT) and proliferation. Together, our in vitro results suggest that PC1 plays an important role in GBM mechanobiology. John Wiley and Sons Inc. 2022-02-01 2022-03 /pmc/articles/PMC8899169/ /pubmed/35106909 http://dx.doi.org/10.1111/jcmm.17212 Text en © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Zoi, Ilianna
Gargalionis, Antonios N.
Papavassiliou, Kostas A.
Nasiri‐Ansari, Narjes
Piperi, Christina
Basdra, Efthimia K.
Papavassiliou, Athanasios G.
Polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro
title Polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro
title_full Polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro
title_fullStr Polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro
title_full_unstemmed Polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro
title_short Polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro
title_sort polycystin‐1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8899169/
https://www.ncbi.nlm.nih.gov/pubmed/35106909
http://dx.doi.org/10.1111/jcmm.17212
work_keys_str_mv AT zoiilianna polycystin1andhydrostaticpressureareimplicatedinglioblastomapathogenesisinvitro
AT gargalionisantoniosn polycystin1andhydrostaticpressureareimplicatedinglioblastomapathogenesisinvitro
AT papavassilioukostasa polycystin1andhydrostaticpressureareimplicatedinglioblastomapathogenesisinvitro
AT nasiriansarinarjes polycystin1andhydrostaticpressureareimplicatedinglioblastomapathogenesisinvitro
AT piperichristina polycystin1andhydrostaticpressureareimplicatedinglioblastomapathogenesisinvitro
AT basdraefthimiak polycystin1andhydrostaticpressureareimplicatedinglioblastomapathogenesisinvitro
AT papavassiliouathanasiosg polycystin1andhydrostaticpressureareimplicatedinglioblastomapathogenesisinvitro