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Article: NADPH oxidase 5α promotes the formation of CD271 tumor-initiating cells in oral cancer

TitleNADPH oxidase 5α promotes the formation of CD271 tumor-initiating cells in oral cancer
Authors
KeywordsNADPH oxidase 5
tumor-initiating cells
cisplatin
natural killer cells
reactive oxygen species
Issue Date2020
PublisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajcr.us
Citation
American Journal of Cancer Research, 2020, v. 10 n. 6, p. 1710-1727 How to Cite?
AbstractOral tongue squamous cell carcinoma (OTSCC) has a distinctive cell sub-population known as tumor-initiating cells (TICs). CD271 is a functional TIC receptor in head and neck cancers. The molecular mechanisms governing CD271 up-regulation remains unclear. Oxidative stress is a contributing factor in TIC development. Here, we explored the potential role of NADPH oxidase 5 (NOX5) and its regulatory mechanism on the development of CD271-expressing OTSCC. Our results showed that the splice variant NOX5α is the most prevalent form expressed in head and neck cancers. NOX5α enhanced OTSCC proliferation, migration, and invasion. Overexpression of NOX5α increased the size of OTSCC xenograft significantly in vivo. The tumor-promoting functions of NOX5α were mediated through the reactive oxygen species (ROS)-generating property. NOX5α activated ERK singling and increased CD271 expression at the transcription level. Also, NOX5α reduces the sensitivity of OTSCC to cisplatin and natural killer cells. The findings indicate that NOX5α plays an important part in the development of TIC in OTSCC.
Persistent Identifierhttp://hdl.handle.net/10722/284784
ISSN
2019 Impact Factor: 5.177
2015 SCImago Journal Rankings: 3.756
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorGao, W-
dc.contributor.authorXu, S-
dc.contributor.authorZhang, M-
dc.contributor.authorLiu, S-
dc.contributor.authorSiu, SPK-
dc.contributor.authorPeng, H-
dc.contributor.authorTsao, GSW-
dc.contributor.authorChan, AWH-
dc.contributor.authorChow, VLY-
dc.contributor.authorChan, JYW-
dc.contributor.authorWong, TS-
dc.contributor.authorNg, JCW-
dc.date.accessioned2020-08-07T09:02:35Z-
dc.date.available2020-08-07T09:02:35Z-
dc.date.issued2020-
dc.identifier.citationAmerican Journal of Cancer Research, 2020, v. 10 n. 6, p. 1710-1727-
dc.identifier.issn2156-6976-
dc.identifier.urihttp://hdl.handle.net/10722/284784-
dc.description.abstractOral tongue squamous cell carcinoma (OTSCC) has a distinctive cell sub-population known as tumor-initiating cells (TICs). CD271 is a functional TIC receptor in head and neck cancers. The molecular mechanisms governing CD271 up-regulation remains unclear. Oxidative stress is a contributing factor in TIC development. Here, we explored the potential role of NADPH oxidase 5 (NOX5) and its regulatory mechanism on the development of CD271-expressing OTSCC. Our results showed that the splice variant NOX5α is the most prevalent form expressed in head and neck cancers. NOX5α enhanced OTSCC proliferation, migration, and invasion. Overexpression of NOX5α increased the size of OTSCC xenograft significantly in vivo. The tumor-promoting functions of NOX5α were mediated through the reactive oxygen species (ROS)-generating property. NOX5α activated ERK singling and increased CD271 expression at the transcription level. Also, NOX5α reduces the sensitivity of OTSCC to cisplatin and natural killer cells. The findings indicate that NOX5α plays an important part in the development of TIC in OTSCC.-
dc.languageeng-
dc.publisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajcr.us-
dc.relation.ispartofAmerican Journal of Cancer Research-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectNADPH oxidase 5-
dc.subjecttumor-initiating cells-
dc.subjectcisplatin-
dc.subjectnatural killer cells-
dc.subjectreactive oxygen species-
dc.titleNADPH oxidase 5α promotes the formation of CD271 tumor-initiating cells in oral cancer-
dc.typeArticle-
dc.identifier.emailGao, W: weigaoi@hku.hk-
dc.identifier.emailSiu, SPK: sharies@hku.hk-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.emailChow, VLY: chowlyv@hku.hk-
dc.identifier.emailChan, JYW: jywchan1@hku.hk-
dc.identifier.emailWong, TS: wongtsa@hkucc.hku.hk-
dc.identifier.authorityGao, W=rp02222-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityChan, JYW=rp01314-
dc.identifier.authorityWong, TS=rp00478-
dc.description.naturepublished_or_final_version-
dc.identifier.pmid32642285-
dc.identifier.pmcidPMC7339284-
dc.identifier.hkuros312324-
dc.identifier.hkuros312148-
dc.identifier.volume10-
dc.identifier.issue6-
dc.identifier.spage1710-
dc.identifier.epage1727-
dc.publisher.placeUnited States-

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