Evidence map›Paper›PMID 34120148›Full record

ArticleCell death & disease2021

H2A.Z acetylation by lincZNF337-AS1 via KAT5 implicated in the transcriptional misregulation in cancer signaling pathway in hepatocellular carcinoma.

Yin Yuan, Wen Cao, Hongbing Zhou, Haixin Qian, Honggang Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 19 citations in OpenAlex.

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  12. miR-196a Promotes Proliferation of Mammary Epithelial Cells by TargetingAnimals : an open access journal from MDPI · 2023
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  16. Epigenetic remodelling in human hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2022
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  18. Article
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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 3 institutions in 1 country.

Yin YuanThe Department of Hepatobiliary Surgery of Hospital Affiliated 5 to Nantong University(Taizhou People's Hospital), Taizhou, Jiangsu Province, China.
Wen CaoThe Department of Liver Disease of Hospital Affiliated 5 to Nantong University(Taizhou People's Hospital), Taizhou, Jiangsu Province, China.
Hongbing ZhouThe Department of Hepatobiliary Surgery of Hospital Affiliated 5 to Nantong University(Taizhou People's Hospital), Taizhou, Jiangsu Province, China.
Haixin QianDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Honggang WangThe Department of General Surgery of Hospital Affiliated 5 to Nantong University(Taizhou People's Hospital), Taizhou, Jiangsu Province, China. 1491763460@qq.com.
Nantong University · CNFirst Affiliated Hospital of Soochow University · CNTaizhou People's Hospital · CN

Funding

Jiangsu Province Postdoctoral Science Foundation 2018M630581Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation) Grants BK 20160572 and BK 20170358
6 · The paper itself

Abstract

In eukaryotes, histones and their variants are essential for chromatin structure and function; both play important roles in the regulation of gene transcription, as well as the development of tumors. We aimed to explore the genomics data of hepatocellular carcinoma (HCC), combined with literature analysis, in terms of the histone variant H2A.Z. Cell phenotype assay confirmed the effect of H2A.Z on the proliferation, metastasis, apoptosis, and cell cycle of HCC cells. H2A.Z was shown to function via the tumor dysregulation signaling pathway, with BCL6 as its interacting protein. In addition, the acetylation level of H2A.Z was higher in HCC and was related to tumor formation. We found the acetylation of H2A.Z to be related to and regulated by lincZNF337-AS1. LincZNF337-AS1 was found to bind to H2A.Z and KAT5 at different sites, promoting the acetylation of H2A.Z through KAT5. We concluded that, in HCC, H2A.Z is an oncogene, whose acetylation promotes the transcription of downstream genes, and is regulated by lincZNF331-AS1.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAcetylationAdultAgedAged, 80 and overAnimalsCase-Control StudiesFemaleGene Expression Regulation, NeoplasticHEK293 CellsHep G2 CellsHistonesHumansLysine Acetyltransferase 5Malehistone H2A.F-ZHistonesKAT5 protein, humanLysine Acetyltransferase 5RNA, Long Noncoding

Identifiers

PMID34120148
PMCPMC8197763
OpenAlexW3168155262

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.