Molecules, Vol. 29, Pages 1708: Antitumoral Activity of the Universal Methyl Donor S-Adenosylmethionine in Glioblastoma Cells

We report here for the first time that AdoMet selectively inhibited the viability and proliferation of U87MG, U343MG, and U251MG GBM cells. In these cell lines, AdoMet induced S and G2/M cell cycle arrest and apoptosis and downregulated the expression and activation of proteins involved in homologous recombination DNA repair, including RAD51, BRCA1, and Chk1. Furthermore, AdoMet was able to maintain DNA in a damaged state, as indicated by the increased γH2AX/H2AX ratio. AdoMet promoted mitotic catastrophe through inhibiting Aurora B kinase expression, phosphorylation, and localization causing GBM cells to undergo mitotic catastrophe-induced death. Finally, AdoMet inhibited DNA repair and induced cell cycle arrest, apoptosis, and mitotic catastrophe in patient-derived GBM cells. In light of these results, AdoMet could be considered a potential adjuvant in GBM therapy.

Source: Molecules - April 10, 2024 Category: Chemistry Authors: Laura Mosca Cristina Pagano Roberta Veglia Tranchese Roberta Grillo Francesca Cadoni Giovanna Navarra Laura Coppola Martina Pagano Luigi Mele Giovanna Cacciapuoti Chiara Laezza Marina Porcelli Tags: Article Source Type: research