Evidence map›Paper›PMID 35121725›Full record

ArticleCell death & disease2022

HBx increases chromatin accessibility and ETV4 expression to regulate dishevelled-2 and promote HCC progression.

Chuqian Zheng, Min Liu, Yanping Ge, Yanyan Qian, Hong Fan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 50 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

5 authors at 1 institution in 1 country.

Chuqian ZhengDepartment of Medical Genetics and Developmental Biology, School of Medicine, The Key Laboratory of Developmental Genes and Human Diseases, Ministry of Education, Southeast University, Nanjing, China.
Min LiuSchool of Life Science and Technology, Southeast University, Nanjing, China.
Yanping GeSchool of Life Science and Technology, Southeast University, Nanjing, China.
Yanyan QianDepartment of Medical Genetics and Developmental Biology, School of Medicine, The Key Laboratory of Developmental Genes and Human Diseases, Ministry of Education, Southeast University, Nanjing, China.
Hong FanDepartment of Medical Genetics and Developmental Biology, School of Medicine, The Key Laboratory of Developmental Genes and Human Diseases, Ministry of Education, Southeast University, Nanjing, China. fanh@seu.edu.cn.ORCID http://orcid.org/0000-0002-2783-7850
Southeast University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81672414National Natural Science Foundation of China (National Science Foundation of China) 81972664
6 · The paper itself

Abstract

Hepatitis B virus (HBV) infection is the predominant causes of hepatocellular carcinoma (HCC). HBV X protein (HBx), as the most frequently integrated viral gene sequence following HBV infection, plays a critical role in the pathogenesis of HCC. H3K27ac is a characteristic marker for identifying active enhancers and even indicates chromatin accessibility associated with super-enhancers (SEs). In this study, H3K27ac ChIP-seq was applied for high-quality SE annotation of HBx-induced SEs and chromatin accessibility evaluation. The results indicated that HBx preferentially affects enrichment of H3K27ac in transcription factor signaling pathway genes, including ETV4. RNA-seq indicated that ETV4 is upregulated by HBx and that upregulated ETV4 promotes HCC progression. Interestingly, ETV4 was also included in the 568 cancer driver gene pool obtained by the Integrative OncoGenomics pipeline. However, the biological function and mechanism of ETV4 remain incompletely understood. In vivo and in vitro, we found that increased ETV4 expression promotes HCC cell migration and invasion by upregulating DVL2 and activating Wnt/β-catenin. The mRNA and protein levels of ETV4 are higher in tumor tissues compared with adjacent tissues, and high expression of ETV4 is associated with poor prognosis in HCC patients. In summary, we first confirm that ETV4 is significantly upregulated by HBx and involved in SE-associated chromatin accessibility. Increased expression of ETV4 promotes HCC cell invasion and metastasis by upregulating DVL2. The present study provides insight into the ETV4-DVL2-β-catenin axis in HBV-related HCC, which will be helpful for treating patients with aggressive HCC.

Indexed as

Carcinoma, HepatocellularDishevelled ProteinsHepatitis BLiver NeoplasmsProto-Oncogene Proteins c-etsbeta CateninCell Line, TumorCell MovementChromatinGene Expression Regulation, NeoplasticHepatitis B virusHep G2 CellsHumansTrans-ActivatorsViral Regulatory and Accessory Proteinsbeta CateninChromatinDishevelled ProteinsDVL2 protein, humanETV4 protein, humanhepatitis B virus X proteinProto-Oncogene Proteins c-etsTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID35121725
PMCPMC8816937
OpenAlexW4210395385

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.