Evidence map›Paper›PMID 35748106›Full record

ArticleCell proliferation2022

DNASE1L3 inhibits proliferation, invasion and metastasis of hepatocellular carcinoma by interacting with β-catenin to promote its ubiquitin degradation pathway.

Bo Li, Yu-Zhen Ge, Wei-Wei Yan, Bin Gong, Kun Cao, Rui Zhao, Chao Li, Ye-Wei Zhang, Yi-Heng Jiang, Shi Zuo

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2022. 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
2.8field-weighted citation impact, top 8% 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, 27 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

10 authors at 3 institutions in 1 country.

Bo LiDepartment of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.ORCID https://orcid.org/0000-0002-9731-2814
Yu-Zhen GeDepartment of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
Wei-Wei YanCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China.
Bin GongCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China.
Kun CaoDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
Rui ZhaoDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
Chao LiDepartment of General Surgery, The First People's Hospital of Fuquan, Fuquan, Guizhou, China.
Ye-Wei ZhangDepartment of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
Yi-Heng JiangDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
Shi ZuoDepartment of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
Guiyang Medical University · CNTCM-Intigrated Cancer Center of Southern Medical University · CNThe First People's Hospital of Guiyang · CN

Funding

Guizhou Medical UniversityNational Natural Science Foundation of ChinaThe 12th Special Fund for Young Scientist of Guizhou Province (2019)5647The National Natural Science Foundation of China (NSFC) Cultivation Program of Affiliated Hospital of Guizhou Medical University gyfynsfc-2021-34
6 · The paper itself

Abstract

As a member of the deoxyribonuclease 1 family, DNASE1L3 plays a significant role both inside and outside the cell. However, the role of DNASE1L3 in hepatocellular carcinoma (HCC) and its molecular basis remains to be further investigated. In this study, we report that DNASE1L3 is downregulated in clinical HCC samples and evaluate the relationship between its expression and HCC clinical features. In vivo and in vitro experiments showed that DNASE1L3 negatively regulates the proliferation, invasion and metastasis of HCC cells. Mechanistic studies showed that DNASE1L3 recruits components of the cytoplasmic β-catenin destruction complex (GSK-3β and Axin), promotes the ubiquitination degradation of β-catenin, and inhibits its nuclear transfer, thus, decreasing c-Myc, P21 and P27 level. Ultimately, cell cycle and EMT signals are restrained. In general, this study provides new insight into the mechanism for HCC and suggests that DNASE1L3 can become a considerable target for HCC.

Indexed as

Carcinoma, HepatocellularLiver Neoplasmsbeta CateninCell Line, TumorCell ProliferationEndodeoxyribonucleasesGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansUbiquitinWnt Signaling Pathwaybeta CateninDNASE1L3 protein, humanEndodeoxyribonucleasesGlycogen Synthase Kinase 3 betaUbiquitin

Identifiers

PMID35748106
PMCPMC9436914
OpenAlexW4283376791

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.