Polycystin-1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro.
Ilianna ZoiAntonios N GargalionisKostas A PapavassiliouNarjes Nasiri-AnsariChristina PiperiEfthimia K BasdraDonatella Delle CavePublished in: Journal of cellular and molecular medicine (2022)
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.
Keyphrases
- cell cycle arrest
- cell proliferation
- transcription factor
- pi k akt
- endoplasmic reticulum stress
- oxidative stress
- induced apoptosis
- cell death
- high glucose
- signaling pathway
- diabetic rats
- single cell
- gene expression
- cell therapy
- protein kinase
- poor prognosis
- endothelial cells
- binding protein
- stem cells
- drug induced
- epithelial mesenchymal transition
- tyrosine kinase
- electronic health record
- cell migration
- cell cycle
- reactive oxygen species
- machine learning
- mesenchymal stem cells
- heat shock
- vascular endothelial growth factor
- optical coherence tomography
- wound healing