Evidence map›Paper›PMID 35092191›Full record

ArticleCancer medicine2022

ZNF191 alters DNA methylation and activates the PI3K-AKT pathway in hepatoma cells via transcriptional regulation of DNMT1.

Yufeng Liu, Hanghang Cheng, Chenchen Cheng, Fengyun Zheng, Zhonghua Zhao, Qi Chen, Wenjiao Zeng, Pingzhao Zhang, Cheng Huang, Wei Jiang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2022. 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
3.2field-weighted citation impact, top 7% 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, 37 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

12 authors at 2 institutions in 2 countries.

Yufeng LiuDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Hanghang ChengDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Chenchen ChengDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Fengyun ZhengInstitutes of Biomedical Sciences, Fudan University, Shanghai, China.
Zhonghua ZhaoDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Qi ChenDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Wenjiao ZengDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Pingzhao ZhangDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Cheng HuangDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Wei JiangKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Xiuping LiuDepartment of Pathology, Shanghai Fifth People's Hospital, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Guoyuan LiuDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.ORCID 0000-0001-9857-283X
Shanghai Medical College of Fudan University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlteration of DNA methylation is an important event in pathogenesis and progression of hepatocellular carcinoma (HCC). DNA methyltransferase (DNMT) 1, the foremost contributor in DNA methylation machinery, was revealed elevated in HCC and significantly correlates with poor prognosis. However, the transcriptional regulation of DNMT1 in HCC remains unknown.

methodsReal-time PCR and immunohistochemistry were performed to detect DNMT1 and zinc finger transcription factor 191 (ZNF191) expressions in HCCs. Transcription activity of DNMT1promoter was analyzed with Luciferase reporter activity assay. The binding capacity of ZNF191 protein to DNMT1 promoter was examined with chromatin immunoprecipitation-qPCR (ChIP-qPCR) and electrophoretic mobility shift assay (EMSA). DNA methylation level of hepatoma cells was detected with Methylation array.

resultsZNF191 can regulate DNMT1 mRNA and protein expression positively, and increase the transcription activity of the DNMT1 promoter. ChIP-qPCR and EMSA revealed that ZNF191 protein directly binds to the DNMT1 promoter at nt-240 AT(TCAT)

conclusionZNF191 is a novel transcription regulator for DNMT1, and the pro-proliferation effect of ZNF191/DNMT1/p-AKT axis in hepatoma cells implies that ZNF191 status in HCCs may affect the therapeutic effect of DNMTs inhibitors and PI3K inhibitors for precise treatment of the disease.

Indexed as

Carcinoma, HepatocellularDNA (Cytosine-5-)-Methyltransferase 1Kruppel-Like Transcription FactorsLiver NeoplasmsCell Line, TumorDNA MethylationHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanKruppel-Like Transcription FactorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktZNF24 protein, humanDNA methylationDNMT1hepatocellular carcinomaPI3K-AKT signaling pathwayzinc finger transcription factor 191(ZNF191)

Identifiers

PMID35092191
PMCPMC8894703
OpenAlexW4210748885

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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.