Evidence map›Paper›PMID 30154409›Full record

ArticleCell death & disease2018

PARP12 (ARTD12) suppresses hepatocellular carcinoma metastasis through interacting with FHL2 and regulating its stability.

Changjuan Shao, Yangyang Qiu, Juan Liu, Huan Feng, Suqin Shen, Hexige Saiyin, Wenbo Yu, Youheng Wei, Long Yu, Wei Su and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

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  12. The roles of FHL2 in cancer.Clinical and experimental medicine · 2023
    Review
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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.

Changjuan ShaoThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Yangyang QiuThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Juan LiuThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Huan FengThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Suqin ShenThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Hexige SaiyinThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Wenbo YuThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Youheng WeiThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Long YuThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Wei SuThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China.
Jiaxue WuThe State Key Laboratory of Genetic Engineering, School of Life Science, Zhongshan Hospital, Fudan University, Shanghai, China. jiaxue@fudan.edu.cn.
Zhongshan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PARP12 is a mono-ADP-ribosyltransferase, but its function remains largely unknown. Here, we identified four-and-a-half LIM-only protein 2 (FHL2) as a functional partner of PARP12 through protein affinity purification. Although PARP12 did not mono-ADP-ribosylate FHL2 in vitro and in vivo, PARP12 deficiency decreased the protein level of FHL2 by promoting its ubiquitination and increased the expression level of transforming growth factor beta1 (TGF-β1), which is independent of PARP12 enzymatic activity. We also provided evidence that PARP12 deficiency increased the migration and invasion of hepatocellular carcinoma (HCC) cells and promoted HCC metastasis in vivo by regulating the epithelial-mesenchymal transition process. These results indicated that PARP12 is a tumor suppressor that plays an important role in HCC metastasis through the regulation of FHL2 stability and TGF-β1 expression.

Indexed as

AnimalsCarcinoma, HepatocellularCell LineCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHEK293 CellsHumansLIM-Homeodomain ProteinsLiver NeoplasmsMaleMiceMuscle ProteinsNeoplasm InvasivenessNeoplasm MetastasisPoly(ADP-ribose) PolymerasesFHL2 protein, humanLIM-Homeodomain ProteinsMuscle ProteinsPARP16 protein, humanPoly(ADP-ribose) PolymerasesTranscription FactorsTransforming Growth Factor beta1Tumor Suppressor Proteins

Identifiers

PMID30154409
PMCPMC6113207
OpenAlexW2889419917

What OpenQuestion holds

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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.