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dc.contributor.authorLiu, Sulai
dc.contributor.authorJiang, Jinqiong
dc.contributor.authorHuang, Linsheng
dc.contributor.authorJiang, Yu
dc.contributor.authorYu, Nanhui
dc.contributor.authorLiu, Xiehong
dc.contributor.authorLv, Yuan
dc.contributor.authorLi, Hao
dc.contributor.authorZou, Lianhong
dc.contributor.authorPeng, Chuang
dc.contributor.authorYu, Xing
dc.contributor.authorJiang, Bo
dc.date.accessioned2020-01-14T03:01:23Z
dc.date.available2020-01-14T03:01:23Z
dc.date.issued2019
dc.identifier.issn1179-1322en_US
dc.identifier.doi10.2147/CMAR.S208773en_US
dc.identifier.urihttp://hdl.handle.net/10072/390219
dc.description.abstractBackground: Inducible nitric oxide synthase (iNOS) has supposed to implicate in inflammation, infection, liver cirrhosis, and neoplastic diseases. This study was designed to explore the biological and clinical function of iNOS in intrahepatic cholangiocarcinoma (ICC). Methods: RT-PCR (Real-time quantitative PCR) and immunohistochemical staining were used to analyze the expression of iNOS in ICC and adjacent tissues. CCK8, transwell assays, flow cytometry were conducted to detect the proliferation, apoptosis, cell cycle. Western blotting was performed to detect the expression of target proteins. Multivariate analyses were conducted to analysis associates between clinicopathological values and survival. Results: We found that levels of iNOS mRNA and protein were dramatically increased in ICC samples and positively correlated with complicated bile duct stone, differentiation, pathology T, pathology M, Wip1, MMP-2, and MMP-9. iNOS expression was significantly correlated with the poor survival of ICC patients. Furthermore, iNOS was high expression in ICC cell lines (QBC-939, ICC-9810, SSP-25) compare with human normal biliary epithelium cell line (HIBEpic); both iNOS knockdown and iNOS inhibitor (1400 W) suppressed cell proliferation, invasion, and migration though nitric oxide production in ICC cells. Down-regulation of iNOS also induced G0/G1 cell cycle arrest and ICC cell apoptosis. Moreover, iNOS knockdown treatment significantly decreased Wip1, MMP-9, and MMP-2 gene expression. Conclusion: Lowly expressed iNOS-inhibited proliferation yet promoted apoptosis of ICC cells. Our data show targeted inhibition of iNOS in ICC may have therapeutic value.en_US
dc.description.peerreviewedYesen_US
dc.languageEnglishen_US
dc.publisherDove Medical Pressen_US
dc.relation.ispartofpagefrom8005en_US
dc.relation.ispartofpageto8022en_US
dc.relation.ispartofjournalCancer Management and Researchen_US
dc.relation.ispartofvolume11en_US
dc.subject.fieldofresearchOncology and Carcinogenesisen_US
dc.subject.fieldofresearchcode1112en_US
dc.subject.keywordsScience & Technologyen_US
dc.subject.keywordsLife Sciences & Biomedicineen_US
dc.subject.keywordsOncologyen_US
dc.subject.keywordsintrahepatic cholangiocarcinomaen_US
dc.subject.keywordsiNOSen_US
dc.titleiNOS is associated with tumorigenicity as an independent prognosticator in human intrahepatic cholangiocarcinomaen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Articlesen_US
dcterms.bibliographicCitationLiu, S; Jiang, J; Huang, L; Jiang, Y; Yu, N; Liu, X; Lv, Y; Li, H; Zou, L; Peng, C; Yu, X; Jiang, B, iNOS is associated with tumorigenicity as an independent prognosticator in human intrahepatic cholangiocarcinoma, Cancer Management and Research, 2019, 11, pp. 8005-8022en_US
dcterms.dateAccepted2019-07-12
dcterms.licensehttps://creativecommons.org/licenses/by-nc/3.0/en_US
dc.date.updated2020-01-14T02:57:33Z
dc.description.versionPublisheden_US
gro.rights.copyright© 2019 Liu et al. This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.en_US
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gro.griffith.authorYu, Xing


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