Please use this identifier to cite or link to this item:
logo share SHARE logo core CORE BASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE

Natural triterpenic diols promote apoptosis in astrocytoma cells through ROS-mediated mitochondrial depolarization and JNK activation

AuthorsMartín, Rubén CSIC; Ibeas, Elvira CSIC; Carvalho-Tavares, Juliana CSIC; Hernández, Marita CSIC ORCID CVN ; Ruiz-Gutiérrez, Valentina CSIC ; Nieto, María Luisa CSIC ORCID
Issue Date22-Jun-2009
PublisherPublic Library of Science
CitationPLoS ONE 4(6): e5975 (2009)
Abstract[Background]: Triterpene alcohols and acids are multifunctional compounds widely distributed throughout the plant kingdom that exhibit a variety of beneficial health properties, being synthetic analogs of oleanolic acid under clinical evaluation as anti-tumoral therapeutic agents. However, the antineoplastic activity of two natural occuring triterpenoid alcohols extracted from olive oil, erythrodiol (an intermediate from oleanolic acid), and its isomer, uvaol, has barely been reported, particularly on brain cancer cells. Astrocytomas are among the most common and aggressive type of primary malignant tumors in the neurological system lacking effective treatments, and in this study, we addressed the effect of these two triterpenic diols on the human 1321N1 astrocytoma cell line.
[Principal Findings]: Erythrodiol and uvaol effectively affected cell proliferation, as well as cell cycle phases and induced 1321N1 cell death. Both triterpenes successfully modulated the apoptotic response, promoting nuclear condensation and fragmentation. They caused retraction and rounding of cultured cells, which lost adherence from their supports, while F-actin and vimentin filaments disappeared as an organized cytoplasmic network. At molecular level, changes in the expression of surface proteins associated with adhesion or death processes were also observed. Moreover, triterpene exposure resulted in the production of reactive oxygen species (ROS) with loss of mitochondrial transmembrane potential, and correlated with the activation of c-Jun N-terminal kinases (JNK). The presence of catalase reversed the triterpenic diols-induced mitochondrial depolarization, JNK activation, and apoptotic death, indicating the critical role of ROS in the action of these compounds.
[Conclusions]: Overall, we provide a significant insight into the anticarcinogenic action of erythrodiol and uvaol that may have a potential in prevention and treatment of brain tumors and other cancers.
Publisher version (URL)
Appears in Collections:(IG) Artículos
(IBGM) Artículos

Files in This Item:
File Description SizeFormat
pone.0005975.pdf856,87 kBAdobe PDFThumbnail
Show full item record
Review this work

Page view(s)

checked on May 20, 2022


checked on May 20, 2022

Google ScholarTM




WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.