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dc.contributor.authorNi, G
dc.contributor.authorChen, S
dc.contributor.authorChen, M
dc.contributor.authorWu, J
dc.contributor.authorYang, B
dc.contributor.authorYuan, J
dc.contributor.authorWalton, SF
dc.contributor.authorLi, H
dc.contributor.authorWei, MQ
dc.contributor.authorWang, Y
dc.contributor.authorChen, G
dc.contributor.authorLiu, X
dc.contributor.authorWang, T
dc.date.accessioned2020-08-31T02:16:18Z
dc.date.available2020-08-31T02:16:18Z
dc.date.issued2020
dc.identifier.issn2296-634X
dc.identifier.doi10.3389/fcell.2020.00676
dc.identifier.urihttp://hdl.handle.net/10072/396911
dc.description.abstractHost defense caerin 1.1 and 1.9 peptides, isolated from the glandular secretion of Australian tree frogs, the genus Litoria, have been previously shown to have multiple biological activities, including the inhibition of human papillomavirus (HPV) 16 early protein E7 transformed murine as well as human cancerous cell proliferation both in vitro and in vivo. However, the mechanism underlying their anti-proliferative activities against HPV18+ cervical cancer HeLa cells remains unknown. This study comparatively investigated the anti-proliferation on HeLa cells by caerin 1.1, 1.9, and their mixture, followed by confocal microscopy examination to assess the cellular intake of the peptides. Tandem mass tag labeling proteomics was employed to reveal the proteins that were significantly regulated by the peptide treatment in cells and cell growth environment, to elucidate the signaling pathways that were modulated. Western blot was performed to confirm the modulation of the pathways. Both caerin 1.1 and 1.9 highly inhibited HeLa cell proliferation with a significant additive effect compared to untreated and control peptide. They entered the cells with different magnitudes. Intensive protein-protein interaction was detected among significantly upregulated proteins. Translation, folding and localization of proteins and RNA processing, apoptosis process was significantly enriched post the treatments. The apoptotic signaling was suggested as a result of tumor necrosis factor-α (TNF-α) pathway activation, indicated by the dose-dependent elevated levels of caspase 3 and caspase 9. The epidermal growth factor receptor and androgen receptor pathways appeared inhibited by the peptides. Moreover, the activation of T-cell receptor derived from the quantitation results further implies the likelihood of recruiting more T cells to the cell growth environment post the treatment and more sensitive to T cell mediated killing of HeLa cells. Our results indicate that caerin 1.1 and 1.9 mediate apoptotic signals of HeLa cells and may subsequently enhances adaptive T cell immune responses.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherFrontiers Media SA
dc.relation.ispartofpagefrom676
dc.relation.ispartofjournalFrontiers in Cell and Developmental Biology
dc.relation.ispartofvolume8
dc.subject.fieldofresearchBiological sciences
dc.subject.fieldofresearchcode31
dc.subject.keywordsHeLa cell
dc.subject.keywordsTMT labeling
dc.subject.keywordsTNF-α signaling pathway
dc.subject.keywordsapoptosis
dc.subject.keywordscaerin peptide
dc.titleHost-Defense Peptides Caerin 1.1 and 1.9 Stimulate TNF-Alpha-Dependent Apoptotic Signals in Human Cervical Cancer HeLa Cells
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationNi, G; Chen, S; Chen, M; Wu, J; Yang, B; Yuan, J; Walton, SF; Li, H; Wei, MQ; Wang, Y; Chen, G; Liu, X; Wang, T, Host-Defense Peptides Caerin 1.1 and 1.9 Stimulate TNF-Alpha-Dependent Apoptotic Signals in Human Cervical Cancer HeLa Cells, Frontiers in Cell and Developmental Biology, 2020, 8, pp. 676-
dcterms.dateAccepted2020-07-03
dcterms.licensehttp://creativecommons.org/licenses/by/4.0/
dc.date.updated2020-08-31T02:07:13Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2020 Ni, Chen, Chen, Wu, Yang, Yuan, Walton, Li, Wei, Wang, Chen, Liu and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
gro.hasfulltextFull Text
gro.griffith.authorChen, Mo
gro.griffith.authorWei, Ming Q.


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