Glioblastoma multiforme (GBM) is characterized by several genetic abnormalities, leading to cell cycle deregulation and abnormal mitosis caused by a defective checkpoint. We previously demonstrated that arecaidine propargyl ester (APE), an orthosteric agonist of M2 muscarinic acetylcholine receptors (mAChRs), arrests the cell cycle of glioblastoma (GB) cells, reducing their survival. The aim of this work was to better characterize the molecular mechanisms responsible for this cell cycle arrest.
M2 Muscarinic receptor activation impairs mitotic progression and bipolar mitotic spindle formation in human glioblastoma cell lines / Di Bari, Maria; Tombolillo, Vanessa; Alessandrini, Francesco; Guerriero, Claudia; Fiore, Mario; Asteriti, Italia Anna; Castigli, Emilia; Sciaccaluga, Miriam; Guarguaglini, Giulia; Degrassi, Francesca; Tata, Ada Maria. - In: CELLS. - ISSN 2073-4409. - 10:7(2021), pp. 1727-1739. [10.3390/cells10071727]
M2 Muscarinic receptor activation impairs mitotic progression and bipolar mitotic spindle formation in human glioblastoma cell lines
Guerriero, Claudia;Asteriti, Italia Anna;Guarguaglini, Giulia;Degrassi, Francesca;Tata, Ada Maria
2021
Abstract
Glioblastoma multiforme (GBM) is characterized by several genetic abnormalities, leading to cell cycle deregulation and abnormal mitosis caused by a defective checkpoint. We previously demonstrated that arecaidine propargyl ester (APE), an orthosteric agonist of M2 muscarinic acetylcholine receptors (mAChRs), arrests the cell cycle of glioblastoma (GB) cells, reducing their survival. The aim of this work was to better characterize the molecular mechanisms responsible for this cell cycle arrest.File | Dimensione | Formato | |
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