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Article: Vanadium Dioxide Nanocoating Induces Tumor Cell Death through Mitochondrial Electron Transport Chain Interruption

TitleVanadium Dioxide Nanocoating Induces Tumor Cell Death through Mitochondrial Electron Transport Chain Interruption
Authors
Keywordsanticancer
charge transfer
functional coatings and films
mitochondria
vanadium dioxide
Issue Date2019
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at https://onlinelibrary.wiley.com/journal/20566646
Citation
Global Challenges, 2019, v. 3 n. 3, p. article no. 1800058 How to Cite?
AbstractA biomaterials surface enabling the induction of tumor cell death is particularly desirable for implantable biomedical devices that directly contact tumor tissues. However, this specific antitumor feature is rarely found. Consequently, an antitumor‐cell nanocoating comprised of vanadium dioxide (VO2) prepared by customized reactive magnetron sputtering has been proposed, and its antitumor‐growth capability has been demonstrated using human cholangiocarcinoma cells. The results reveal that the VO2 nanocoating is able to interrupt the mitochondrial electron transport chain and then elevate the intracellular reactive oxygen species levels, leading to the collapse of the mitochondrial membrane potential and the destruction of cell redox homeostasis. Indeed, this chain reaction can effectively trigger oxidative damage in the cholangiocarcinoma cells. Additionally, this study has provided new insights into designing a tumor‐cell‐inhibited biomaterial surface, which is modulated by the mechanism of mitochondria‐targeting tumor cell death.
Persistent Identifierhttp://hdl.handle.net/10722/278239
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLI, J-
dc.contributor.authorJIANG, M-
dc.contributor.authorZHOU, H-
dc.contributor.authorJIN, P-
dc.contributor.authorCheung, KMC-
dc.contributor.authorCHU, PK-
dc.contributor.authorYeung, KWK-
dc.date.accessioned2019-10-04T08:10:10Z-
dc.date.available2019-10-04T08:10:10Z-
dc.date.issued2019-
dc.identifier.citationGlobal Challenges, 2019, v. 3 n. 3, p. article no. 1800058-
dc.identifier.issn2056-6646-
dc.identifier.urihttp://hdl.handle.net/10722/278239-
dc.description.abstractA biomaterials surface enabling the induction of tumor cell death is particularly desirable for implantable biomedical devices that directly contact tumor tissues. However, this specific antitumor feature is rarely found. Consequently, an antitumor‐cell nanocoating comprised of vanadium dioxide (VO2) prepared by customized reactive magnetron sputtering has been proposed, and its antitumor‐growth capability has been demonstrated using human cholangiocarcinoma cells. The results reveal that the VO2 nanocoating is able to interrupt the mitochondrial electron transport chain and then elevate the intracellular reactive oxygen species levels, leading to the collapse of the mitochondrial membrane potential and the destruction of cell redox homeostasis. Indeed, this chain reaction can effectively trigger oxidative damage in the cholangiocarcinoma cells. Additionally, this study has provided new insights into designing a tumor‐cell‐inhibited biomaterial surface, which is modulated by the mechanism of mitochondria‐targeting tumor cell death.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at https://onlinelibrary.wiley.com/journal/20566646-
dc.relation.ispartofGlobal Challenges-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectanticancer-
dc.subjectcharge transfer-
dc.subjectfunctional coatings and films-
dc.subjectmitochondria-
dc.subjectvanadium dioxide-
dc.titleVanadium Dioxide Nanocoating Induces Tumor Cell Death through Mitochondrial Electron Transport Chain Interruption-
dc.typeArticle-
dc.identifier.emailCheung, KMC: cheungmc@hku.hk-
dc.identifier.emailYeung, KWK: wkkyeung@hku.hk-
dc.identifier.authorityCheung, KMC=rp00387-
dc.identifier.authorityYeung, KWK=rp00309-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1002/gch2.201800058-
dc.identifier.hkuros307079-
dc.identifier.volume3-
dc.identifier.issue3-
dc.identifier.spagearticle no. 1800058-
dc.identifier.epagearticle no. 1800058-
dc.identifier.isiWOS:000460185600002-
dc.publisher.placeUnited States-

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