Evidence map›Paper›PMID 31874246›Full record

ArticleCancer letters2020

ZBP-89 negatively regulates self-renewal of liver cancer stem cells via suppression of Notch1 signaling pathway.

Nuozhou Wang, Ming-Yue Li, Yi Liu, Jianqing Yu, Jianwei Ren, Zhiyuan Zheng, Shanshan Wang, Shucai Yang, Sheng-Li Yang, Li-Ping Liu and 5 more

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 40 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 7 institutions in 2 countries.

Nuozhou WangDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Ming-Yue LiDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China; Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, Guangdong, China.
Yi LiuDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China; Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical University, Zhanjiang, Guangdong, China.
Jianqing YuDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Jianwei RenDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Zhiyuan ZhengDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Shanshan WangSchool of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, China.
Shucai YangDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China; Department of Clinical Laboratory, Pingshan District People's Hospital of Shenzhen, Shenzhen, Guangdong, China.
Sheng-Li YangCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Li-Ping LiuDepartment of Hepatobiliary and Pancreas Surgery, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), Shenzhen, Guangdong Province, China.
Bao-Guang HuDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Binzhou Medical University, Binzhou, Shandong, China.
Charing Cn ChongDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Juanita L MerchantDivision of Gastroenterology, Division of Gastroenterology & Hepatology, University of Arizona College of Medicine, PO Box 245028, 1501 N. Campbell Ave, Tucson, AZ, 85724-5028, USA.
Paul Bs LaiDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China. Electronic address: paullai@surgery.cuhk.edu.hk.
George Gong ChenDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China; Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical University, Zhanjiang, Guangdong, China; Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, Guangdong, China. Electronic address: gchen@cuhk.edu.hk.
Chinese University of Hong Kong · CNPrince of Wales Hospital · CNUnion Hospital · CNBinzhou University · CNGuangdong Pharmaceutical University · CNJinan University · CNUniversity of Arizona · US

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OMARY, BISHR · 1986 to 2021
$22.5M
Mechanisms of Gastrointestional Growth &TransformationR01DK055732 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 2000 to 2014
$4.1M
Mechanisms of Gastrointestinal Growth and TransformationR56DK055732 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 2010 to 2010
$369k
NIDDK NIH HHS P30 DK034933NIDDK NIH HHS R01 DK055732NIDDK NIH HHS R56 DK055732
6 · The paper itself

Abstract

Liver 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 stemness 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 stemness via inhibiting the Notch1 signaling.

Indexed as

AnimalsBiomarkers, TumorCell Line, TumorCell Self RenewalDisease-Free SurvivalDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHeterograftsHumansLiverLiver NeoplasmsMaleMiceNeoplastic Stem CellsReceptor, Notch1Biomarkers, TumorDNA-Binding ProteinsMAML1 protein, humanNOTCH1 protein, humanReceptor, Notch1Transcription FactorsZNF148 protein, humanHepatocellular carcinomaLiver cancer stemnessNotch1RecurrenceZBP-89

Identifiers

PMID31874246
PMCPMC7226908
OpenAlexW2998186877

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.