Evidence map›Paper›PMID 35950456›Full record

ArticleMolecules and cells2022

Downregulation of SETD5 Suppresses the Tumorigenicity of Hepatocellular Carcinoma Cells.

Mijin Park, Byul Moon, Jong-Hwan Kim, Seung-Jin Park, Seon-Kyu Kim, Kihyun Park, Jaehoon Kim, Seon-Young Kim, Jeong-Hoon Kim, Jung-Ae Kim

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Molecules and cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Mijin ParkDepartment of Functional Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology, Daejeon 34113, Korea.ORCID 0000-0003-1643-2548
Byul MoonDepartment of Functional Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology, Daejeon 34113, Korea.ORCID 0000-0003-3969-3732
Jong-Hwan KimKorea Bioinformation Center, KRIBB, Daejeon 34141, Korea.ORCID 0000-0002-9520-0771
Seung-Jin ParkDepartment of Functional Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology, Daejeon 34113, Korea.ORCID 0000-0003-0666-605X
Seon-Kyu KimDepartment of Functional Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology, Daejeon 34113, Korea.ORCID 0000-0002-4176-5187
Kihyun ParkDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.ORCID 0000-0001-7841-624X
Jaehoon KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.ORCID 0000-0003-4035-0438
Seon-Young KimDepartment of Functional Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology, Daejeon 34113, Korea.ORCID 0000-0002-1030-7730
Jeong-Hoon KimDepartment of Functional Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology, Daejeon 34113, Korea.ORCID 0000-0001-6338-7175
Jung-Ae KimDepartment of Functional Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology, Daejeon 34113, Korea.ORCID 0000-0001-5485-4843
Korea Advanced Institute of Science and Technology · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is an aggressive and incurable cancer. Although understanding of the molecular pathogenesis of HCC has greatly advanced, therapeutic options for the disease remain limited. In this study, we demonstrated that SETD5 expression is positively associated with poor prognosis of HCC and that SETD5 depletion decreased HCC cell proliferation and invasion while inducing cell death. Transcriptome analysis revealed that SETD5 loss downregulated the interferon-mediated inflammatory response in HCC cells. In addition, SETD5 depletion downregulated the expression of a critical glycolysis gene, PKM (pyruvate kinase M1/2), and decreased glycolysis activity in HCC cells. Finally, SETD5 knockdown inhibited tumor growth in xenograft mouse models. These results collectively suggest that SETD5 is involved in the tumorigenic features of HCC cells and that targeting SETD5 may suppress HCC progression.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsCarcinogenesisCell Line, TumorCell ProliferationDown-RegulationGene Expression Regulation, NeoplasticHumansMethyltransferasesMiceMethyltransferasesSETD5 protein, humanepigeneticsglycolysishepatocellular carcinomahistone lysine methyltransferaseinterferon responseSETD5

Identifiers

PMID35950456
PMCPMC9385566
OpenAlexW4291015002

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.