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dc.contributor.authorWang, Nuozhou
dc.contributor.authorLi, Ming-Yue
dc.contributor.authorLiu, Yi
dc.contributor.authorYu, Jianqing
dc.contributor.authorRen, Jianwei
dc.contributor.authorZheng, Zhiyuan
dc.contributor.authorWang, Shanshan
dc.contributor.authorYang, Shucai
dc.contributor.authorYang, Sheng-Li
dc.contributor.authorLiu, Li-Ping
dc.contributor.authorHu, Bao-Guang
dc.contributor.authorChong, Charing Cn
dc.contributor.authorMerchant, Juanita L
dc.contributor.authorLai, Paul Bs
dc.contributor.authorChen, George Gong
dc.date.accessioned2020-02-26T18:08:43Z
dc.date.available2020-02-26T18:08:43Z
dc.date.issued2019-12-23
dc.identifier.citationWang, N., Li, M. Y., Liu, Y., Yu, J., Ren, J., Zheng, Z., ... & Hu, B. G. (2020). ZBP-89 negatively regulates self-renewal of liver cancer stem cells via suppression of Notch1 signaling pathway. Cancer Letters, 472, 70-80.en_US
dc.identifier.issn0304-3835
dc.identifier.pmid31874246
dc.identifier.doi10.1016/j.canlet.2019.12.026
dc.identifier.urihttp://hdl.handle.net/10150/637658
dc.description.abstractLiver cancer stem cells (LCSCs) initiate hepatocellular carcinoma (HCC) and contribute to its recurrence and treatment resistance. Studies have suggested ZBP-89 as a candidate tumor suppressor in HCC. We explored the role of ZBP-89 in the regulation of LCSCs. This study was performed in liver tissue samples from 104 HCC patients, 2 cell lines and mouse tumor models. We demonstrated that ZBP-89 was weakly expressed in LCSCs. Patients with high expression of LCSC markers displayed reduced survivals and higher recurrence rates after curative surgical operation. The expression of ZBP-89 was predictive for decreased recurrence. LCSC markers were negatively correlated with ZBP-89 in HCC tissues and in enriched liver tumor spheres. The exogenous expression of ZBP-89 attenuated the tumor-sphere formation and secondary colony formation capabilities of LCSCs in vitro and tumorigenicity in vivo. Furthermore, the negative effect of ZBP-89 on cancer sternness was Notch1-dependent. Localized with Notch1 intracellular domain (NICD1) in the nucleus, ZBP-89 repressed the Notch1 signaling pathway by competitive binding to NICD1 with MAML1. Collectively, ZBP-89 negatively regulates HCC sternness via inhibiting the Notch1 signaling.en_US
dc.language.isoenen_US
dc.publisherELSEVIER IRELAND LTDen_US
dc.rightsCopyright © 2019 Elsevier B.V. All rights reserved.en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.subjectHepatocellular carcinomaen_US
dc.subjectLiver cancer stemnessen_US
dc.subjectNotch1en_US
dc.subjectRecurrenceen_US
dc.subjectZBP-89en_US
dc.titleZBP-89 negatively regulates self-renewal of liver cancer stem cells via suppression of Notch1 signaling pathwayen_US
dc.typeArticleen_US
dc.identifier.eissn1872-7980
dc.contributor.departmentUniv Arizona, Coll Med, Div Gastroenterol & Hepatolen_US
dc.identifier.journalCancer lettersen_US
dc.description.note12 month embargo; available online 23 December 2019.en_US
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en_US
dc.eprint.versionFinal accepted manuscripten_US
dc.source.journaltitleCancer letters
dc.source.volume472
dc.source.beginpage70
dc.source.endpage80
dc.source.countryIreland


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