Evidence map›Paper›PMID 31432592›Full record

ArticleCancer science2019

G9a and histone deacetylases are crucial for Snail2-mediated E-cadherin repression and metastasis in hepatocellular carcinoma.

Yue Hu, Yayuan Zheng, Mingrui Dai, Xueju Wang, Jiaxin Wu, Bin Yu, Haihong Zhang, Yinqiu Cui, Wei Kong, Hui Wu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

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  6. Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025
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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

11 authors at 2 institutions in 1 country.

Yue HuNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
Yayuan ZhengNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
Mingrui DaiNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
Xueju WangPathology Department, China-Japan Union Hospital of Jilin University, Changchun, China.
Jiaxin WuNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
Bin YuNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
Haihong ZhangNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
Yinqiu CuiSchool of Life Sciences, Jilin University, Changchun, China.
Wei KongNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
Hui WuNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.ORCID https://orcid.org/0000-0002-3068-3805
Xianghui YuNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China.
Jilin University · CNUnion Hospital · CN

Funding

China Postdoctoral Science Foundation 2019TQ0114National Natural Science Foundation of China 81301803
6 · The paper itself

Abstract

Functional E-cadherin loss, a hallmark of epithelial-mesenchymal transition (EMT), is important for metastasis. However, the mechanism of Snail2 in hepatocellular carcinoma (HCC) EMT and metastasis remains unclear. Here, we showed that Snail2 was upregulated in primary HCC, and significantly increased during transforming growth factor-β-induced liver cell EMT. Snail2-overexpressing and knockdown cell lines have been established to determine its function in EMT in HCC. H3K9 methylation was upregulated and H3K4 and H3K56 acetylation were downregulated at the E-cadherin promoter in Snail2-overexpressing cancer cells. Furthermore, Snail2 interacted with G9a and histone deacetylases (HDACs) to form a complex to suppress E-cadherin transcription. Snail2 overexpression enhanced migration and invasion in HCC cells, whereas G9a and HDAC inhibition significantly reversed this effect. Moreover, Snail2 overexpression in cancer cells increased tumor metastasis and shortened survival time in mice, whereas G9a and HDAC inhibitors extended survival. Our study not only reveals a critical mechanism underlying the epigenetic regulation of EMT but also suggests novel treatment strategies for HCC.

Indexed as

Epigenesis, GeneticAcetylationAnimalsAzepinesCadherinsCarcinoma, HepatocellularCell MovementDisease ProgressionDown-RegulationEpithelial-Mesenchymal TransitionFemaleHistocompatibility AntigensHistone Deacetylase InhibitorsHistone DeacetylasesHistone-Lysine N-MethyltransferaseHumansAzepinesBIX 01294CadherinsEHMT2 protein, humanHistocompatibility AntigensHistone Deacetylase InhibitorsHistone DeacetylasesHistone-Lysine N-MethyltransferaseHydroxamic AcidsQuinazolinesSNAI1 protein, humanSnail Family Transcription FactorsTransforming Growth Factor betatrichostatin Aepithelial-mesenchymal transitionG9aHDAChepatocellular carcinomaSnail2

Identifiers

PMID31432592
PMCPMC6825017
OpenAlexW2969500562

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.