Evidence map›Paper›PMID 29653560›Full record

ArticleBMC cancer2018

ZBP-89 and Sp1 contribute to Bak expression in hepatocellular carcinoma cells.

Xia Kong, Pin Xu, Wei-Jie Cai, Huai-Gao Wang, Bin-Bin Li, Guo-Liang Huang, Zhi-Wei He, George Chen, Cai-Guo Ye

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

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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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Regulation of apoptosis by ubiquitination in liver cancer.American journal of cancer research · 2023
    Review
  5. Article
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  7. Article
  8. Transcriptional regulation of the porcine miR-17-92 cluster.Molecular genetics and genomics : MGG · 2019
    Article
  9. Targeting Transcription Factors for Cancer Treatment.Molecules (Basel, Switzerland) · 2018
    Review
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

9 authors at 2 institutions in 2 countries.

Xia KongChina-America Cancer Research Institute, Guangdong Medical University, Guangzhou, Guangdong Province, China.
Pin XuChina-America Cancer Research Institute, Guangdong Medical University, Guangzhou, Guangdong Province, China.
Wei-Jie CaiChina-America Cancer Research Institute, Guangdong Medical University, Guangzhou, Guangdong Province, China.
Huai-Gao WangChina-America Cancer Research Institute, Guangdong Medical University, Guangzhou, Guangdong Province, China.
Bin-Bin LiChina-America Cancer Research Institute, Guangdong Medical University, Guangzhou, Guangdong Province, China.
Guo-Liang HuangChina-America Cancer Research Institute, Guangdong Medical University, Guangzhou, Guangdong Province, China.
Zhi-Wei HeChina-America Cancer Research Institute, Guangdong Medical University, Guangzhou, Guangdong Province, China.
George ChenDepartment of Surgery, The Chinese University of Hong Kong, Hong Kong, SAR, China.
Cai-Guo YeChina-America Cancer Research Institute, Guangdong Medical University, Guangzhou, Guangdong Province, China. yecaiguo@gdmu.edu.cn.ORCID 0000-0002-0401-4245
Guangdong Medical College · CNChinese University of Hong Kong · HK

Funding

Special Talent Supportive Grant 4TZ160001Gthe National Natural Science Foundation of China 81572782
6 · The paper itself

Abstract

backgroundKruppel family member zinc binding protein 89 (ZBP-89), also known as ZNF148, regulates Bak expression via binding to GC-rich promoter domain. It is not clear if other GC-rich binding factors, such as Sp family members, can interact with ZBPp-89 on Bak expression. This study aims to elucidate the mechanism of Bak expression regulation by ZBP-89 and Sp proteins, based on in vitro experiment and The Cancer Genome Atlas (TCGA) hepatocellular carcinoma (HCC) data cohort.

methodsWe downloaded TCGA hepatocellular carcinoma (HCC) cohort data to analysis the association of Bak transcription level with ZBP-89 and Sp proteins transcription level. HCC cell lines and liver immortal non-tumour cell lines were used for mechanism study, including western blotting analysis, expression vector mediated gene expression and siRNA interference.

resultsResults showed that cancer tissues have higher Bak transcription level compared with adjacent non-cancer tissues. Bak transcription level was correlated with Sp1 and Sp3 expression level, while no correlation was found in ZBP-89 and Bak, neither Sp2 nor Sp4. Mithramycin A (MMA) induced Bak expression in a dose-dependent manner. Western blotting results showed Sp1 overexpression increased Bak expression both in liver immortal non-tumour cells and HCC cells. Interference Sp1 expression could inhibit Bak expression alone. ZBP-89 siRNA suppressed Bak expression even in the presence of MMA treatment and S1 overexpression. Additionally, Bak and Sp1 level were associated with HCC patient survival.

conclusionsBak expression required ZBP-89 and Sp1 cooperative regulation simultaneously.

Indexed as

Gene Expression Regulation, Neoplasticbcl-2 Homologous Antagonist-Killer ProteinCarcinoma, HepatocellularCell Line, TumorCohort StudiesDNA-Binding ProteinsHumansKaplan-Meier EstimateLiver NeoplasmsPromoter Regions, GeneticProtein BindingRNA InterferenceRNA, MessengerRNA, Small InterferingSp1 Transcription FactorSp3 Transcription FactorBAK1 protein, humanbcl-2 Homologous Antagonist-Killer ProteinDNA-Binding ProteinsRNA, MessengerRNA, Small InterferingSp1 Transcription FactorSp3 Transcription FactorTranscription FactorsZNF148 protein, humanBakHepatocellular carcinomaSp1Sp3ZBP-89

Identifiers

PMID29653560
PMCPMC5899329
OpenAlexW2803646425

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LicenceCC BY
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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.