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Article: Dioscin induces cancer cell apoptosis through elevated oxidative stress mediated by downregulation of peroxiredoxins

TitleDioscin induces cancer cell apoptosis through elevated oxidative stress mediated by downregulation of peroxiredoxins
Authors
KeywordsApoptosis
Dioscin
Esophageal cancer
Peroxiredoxins
Reactive oxygen species
Issue Date2012
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.php
Citation
Cancer Biology And Therapy, 2012, v. 13 n. 3, p. 137-147 How to Cite?
AbstractDioscin has been shown to promote anticancer activity against several forms of cancers. However, its detailed molecular mechanisms have not been clarified. In this study, we demonstrate that dioscin induces apoptosis in cancer cells through the induction of oxidative stress. Treatment with cancer cells in vitro with dioscin resulted in rapid generation of reactive oxygen species (ROS) and the induction of mitochondrial pathway apoptosis in human esophageal cancer cell line Kyse510. Inhibition of oxidative stress by the antioxidant N-acetylcysteine blocked the induction of apoptosis by dioscin, indicating that ROS generation is the primary mechanism responsible for the proapoptotic activity of dioscin. Proteomic analysis and protein gel blotting further revealed peroxiredoxins 1and 6 (PRDX 1 and 6), which are implicated in ROS metabolism and apoptosis, were associated with the anticancer effects of dioscin. Meanwhile, overexpression of PRDX 1 and 6 significantly blocked the elevated ROS and apoptosis induced by dioscin. In conclusion, we suggest that PRDX1 and PRDX6 are key targets in the process of dioscin-induced apoptosis that involves intracellular elevated ROS.
Persistent Identifierhttp://hdl.handle.net/10722/145554
ISSN
2015 Impact Factor: 2.921
2015 SCImago Journal Rankings: 1.297
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China30371761
Funding Information:

We thank Vicki Geall of the Research Services Section of The University of Hong Kong for editorial assistance. This work was supported in part by the National Natural Science Foundation of China (Grant No. 30371761).

References

 

DC FieldValueLanguage
dc.contributor.authorWang, Zen_HK
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorWang, Nen_HK
dc.contributor.authorWang, DMen_HK
dc.contributor.authorLi, YWen_HK
dc.contributor.authorHan, Fen_HK
dc.contributor.authorShen, JGen_HK
dc.contributor.authorYang, DPen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorChen, JPen_HK
dc.date.accessioned2012-02-28T01:53:55Z-
dc.date.available2012-02-28T01:53:55Z-
dc.date.issued2012en_HK
dc.identifier.citationCancer Biology And Therapy, 2012, v. 13 n. 3, p. 137-147en_HK
dc.identifier.issn1538-4047en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145554-
dc.description.abstractDioscin has been shown to promote anticancer activity against several forms of cancers. However, its detailed molecular mechanisms have not been clarified. In this study, we demonstrate that dioscin induces apoptosis in cancer cells through the induction of oxidative stress. Treatment with cancer cells in vitro with dioscin resulted in rapid generation of reactive oxygen species (ROS) and the induction of mitochondrial pathway apoptosis in human esophageal cancer cell line Kyse510. Inhibition of oxidative stress by the antioxidant N-acetylcysteine blocked the induction of apoptosis by dioscin, indicating that ROS generation is the primary mechanism responsible for the proapoptotic activity of dioscin. Proteomic analysis and protein gel blotting further revealed peroxiredoxins 1and 6 (PRDX 1 and 6), which are implicated in ROS metabolism and apoptosis, were associated with the anticancer effects of dioscin. Meanwhile, overexpression of PRDX 1 and 6 significantly blocked the elevated ROS and apoptosis induced by dioscin. In conclusion, we suggest that PRDX1 and PRDX6 are key targets in the process of dioscin-induced apoptosis that involves intracellular elevated ROS.en_HK
dc.languageengen_US
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.phpen_HK
dc.relation.ispartofCancer Biology and Therapyen_HK
dc.subjectApoptosisen_HK
dc.subjectDioscinen_HK
dc.subjectEsophageal canceren_HK
dc.subjectPeroxiredoxinsen_HK
dc.subjectReactive oxygen speciesen_HK
dc.subject.meshAntineoplastic Agents - pharmacology-
dc.subject.meshApoptosis - drug effects-
dc.subject.meshDiosgenin - analogs and derivatives - pharmacology-
dc.subject.meshDown-Regulation - drug effects-
dc.subject.meshPeroxiredoxins - genetics - metabolism-
dc.titleDioscin induces cancer cell apoptosis through elevated oxidative stress mediated by downregulation of peroxiredoxinsen_HK
dc.typeArticleen_HK
dc.identifier.emailShen, JG: shenjg@hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.emailChen, JP: abchen@hku.hken_HK
dc.identifier.authorityShen, JG=rp00487en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.authorityChen, JP=rp01316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.4161/cbt.13.3.18693en_HK
dc.identifier.pmid22231406-
dc.identifier.scopuseid_2-s2.0-84863131822en_HK
dc.identifier.scopuseid_2-s2.0-84862243614-
dc.identifier.hkuros198779en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84863131822&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue3en_HK
dc.identifier.spage137en_HK
dc.identifier.epage147en_HK
dc.identifier.isiWOS:000300359400003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Z=7410054221en_HK
dc.identifier.scopusauthoridCheng, Y=55251338100en_HK
dc.identifier.scopusauthoridWang, N=55251266100en_HK
dc.identifier.scopusauthoridWang, DM=36955783900en_HK
dc.identifier.scopusauthoridLi, YW=55008616700en_HK
dc.identifier.scopusauthoridHan, F=23569225000en_HK
dc.identifier.scopusauthoridShen, JG=7404929947en_HK
dc.identifier.scopusauthoridYang, DP=8901049400en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridChen, JP=22733695400en_HK

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