Journal
FRONTIERS IN ONCOLOGY
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2023.1143664
Keywords
glioblastoma; 5-Demethylnobiletin; cell cycle arrest; cell apoptosis; ERK1; 2; AKT; STAT3
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5-Demethylnobiletin, an active ingredient in citrus polymethoxyflavones, was found to inhibit the proliferation of various tumor cells. This study explored its anti-tumor effect on glioblastoma and its molecular mechanisms. The results showed that 5-Demethylnobiletin significantly inhibited the viability, migration, and invasion of glioblastoma cells. It induced cell cycle arrest at the G0/G1 phase and apoptosis by regulating various proteins and inhibiting specific signaling pathways. The in vivo model also confirmed its inhibitory effect on U87-MG cell growth. Therefore, 5-Demethylnobiletin holds promise as a potential glioblastoma treatment drug.
5-Demethylnobiletin is the active ingredient in citrus polymethoxyflavones that could inhibit the proliferation of several tumor cells. However, the anti-tumor effect of 5-Demethylnobiletin on glioblastoma and the underlying molecular mechanisms are remains unknown. In our study, 5-Demethylnobiletin markedly inhibited the viability, migration and invasion of glioblastoma U87-MG, A172 and U251 cells. Further research revealed that 5-Demethylnobiletin induces cell cycle arrest at the G0/G1 phase in glioblastoma cells by downregulating Cyclin D1 and CDK6 expression levels. Furthermore, 5-Demethylnobiletin significantly induced glioblastoma cells apoptosis by upregulating the protein levels of Bax and downregulating the protein level of Bcl-2, subsequently increasing the expression of cleaved caspase-3 and cleaved caspase-9. Mechanically, 5-Demethylnobiletin trigged G0/G1 phase arrest and apoptosis by inhibiting the ERK1/2, AKT and STAT3 signaling pathway. Furthermore, 5-Demethylnobiletin inhibition of U87-MG cell growth was reproducible in vivo model. Therefore, 5-Demethylnobiletin is a promising bioactive agent that might be used as glioblastoma treatment drug.
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