Auraptene-induced cytotoxicity mechanisms in human malignant glioblastoma (U87) cells
dc.contributor.author | Afshari, Amir R. | |
dc.contributor.author | Jalili-Nik, Mohammad | |
dc.contributor.author | Soukhtanloo, Mohammad | |
dc.contributor.author | Ghorbani, Ahmad | |
dc.contributor.author | Sadeghnia, Hamid R. | |
dc.contributor.author | Mollazadeh, Hamid | |
dc.contributor.author | Karimi Roshan, Mostafa | |
dc.contributor.author | Rahmani, Farzad | |
dc.contributor.author | Sabri, Hamed | |
dc.contributor.author | Vahedi, Mohammad Mahdi | |
dc.contributor.author | Mousavi, Seyed Hadi | |
dc.date.accessioned | 2020-02-28T11:38:58Z | |
dc.date.available | 2020-02-28T11:38:58Z | |
dc.date.issued | 2019-07-30 | |
dc.description.abstract | Glioblastoma multiforme (GBM), like the devastating type of astrocytic tumors, is one of the most challenging cancers to treat owing to its aggressive nature. Auraptene, as a prenyloxy coumarin from citrus species, represents antioxidant and antitumor activities; however, the underlying antitumor mechanisms of auraptene against GBM remain unclear. The present study aimed to evaluate the cytotoxic and apoptogenic effect s of auraptene, as a promising natural product, and the possible signaling pathways affected in human malignant GBM (U87) cells. Reactive oxygen species (ROS) production significantly decreased in the first 2, and 6 hours after treatment with auraptene however, ROS levels increased in other incubation times (8 and 24 hours), dramatically. N-acetyl-cysteine (NAC) markedly attenuated auraptene–induced ROS production, and consequently reversed auraptene–induced cytotoxicity in 8 and 24 hours after treatment, as well. Induction of apoptosis occurred in the first 24- and 48-hours concentration-dependently. The qRT-PCR showed an up-regulation in p21, CXCL3, and a down-regulation in Cyclin D1 genes expression. Western blot analysis confirmed the up-regulation of the Bax/Bcl-2 ratio protein levels concentration-dependently. Hence, this study collectively revealed that the increase in ROS level is at least one of the mechanisms associated with auraptene-induced GBM cell toxicity as well as the induction of apoptosis through Bax/Bcl-2 modulation and genes expression involved that contribute to the cytotoxicity of auraptene in U87 cells. So, auraptene might be utilized as a potential novel anti-GBM agent after further studies. | en |
dc.identifier.issn | 1611-2156 | |
dc.identifier.uri | http://hdl.handle.net/2003/39016 | |
dc.identifier.uri | http://dx.doi.org/10.17877/DE290R-20935 | |
dc.language.iso | en | |
dc.relation.ispartofseries | EXCLI Journal;Vol. 18 2019 | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.subject | Glioblastoma multiforme | en |
dc.subject | Auraptene | en |
dc.subject | ROS | en |
dc.subject | Apoptosis | en |
dc.subject.ddc | 610 | |
dc.title | Auraptene-induced cytotoxicity mechanisms in human malignant glioblastoma (U87) cells | en |
dc.title.alternative | role of reactive oxygen species (ROS) | en |
dc.type | Text | |
dc.type.publicationtype | article | |
dcterms.accessRights | open access | |
eldorado.dnb.zdberstkatid | 2132560-1 | |
eldorado.secondarypublication | true |