Evidence map›Paper›PMID 38317186›Full record

ArticleJournal of experimental & clinical cancer research : CR2024

PARD3 drives tumorigenesis through activating Sonic Hedgehog signalling in tumour-initiating cells in liver cancer.

Junyu Wu, Hor-Yue Tan, Yau-Tuen Chan, Yuanjun Lu, Zixin Feng, Hongchao Yuan, Cheng Zhang, Yibin Feng, Ning Wang

Abstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  15. Frontiers in pharmacology · 2024
    Review
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

9 authors.

Junyu Wu *School of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Hor-Yue Tan *School of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Yau-Tuen ChanSchool of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Yuanjun LuSchool of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Zixin FengSchool of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Hongchao YuanSchool of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Cheng ZhangSchool of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Yibin FengSchool of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Ning WangSchool of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. ckwang@hku.hk.

Funding

Innovation and Technology Fund PRP/028/22FXResearch Grants Committee (RGC) of Hong Kong, HKSAR 17119621Research Grants Committee (RGC) of Hong Kong, HKSAR 17121419the Health and Medical Research Fund 18192141the Health and Medical Research Fund 19200701the Health and Medical Research Fund 19201951the Health@InnoHK Initiative Fund of the Hong Kong Special Administrative Region Government ITC RC/IHK/4/7
6 · The paper itself

Abstract

backgroundPar-3 Family Cell Polarity Regulator (PARD3) is a cellular protein essential for asymmetric cell division and polarized growth. This study aimed to study the role of PARD3 in hepatic tumorigenesis.

methodsThe essential role of PARD3 in mediating hepatic tumorigenesis was assessed in diet-induced spontaneous liver tumour and syngeneic tumour models. The mechanism of PARD3 was delineated by bulk and single-cell RNA sequencing. The clinical significance of PARD3 was identified by tissue array analysis.

resultsPARD3 was overexpressed in tumour tissues and PARD3 overexpression was positively correlated with high tumour stage as well as the poor prognosis in patients. In models of spontaneous liver cancer induced by choline-deficient, amino acid-defined (CDAA) and methionine-choline-deficient (MCD) diets, upregulation of PARD3 was induced specifically at the tumorigenesis stage rather than other early stages of liver disease progression. Site-directed knockout of PARD3 using an adeno-associated virus 8 (AAV8)-delivered CRISPR/Cas9 single-guide RNA (sgRNA) plasmid blocked hepatic tumorigenesis, while PARD3 overexpression accelerated liver tumour progression. In particular, single-cell sequencing analysis suggested that PARD3 was enriched in primitive tumour cells and its overexpression enhanced tumour-initiating cell (TICs). Overexpression of PARD3 maintained the self-renewal ability of the CD133

conclusionThis study revealed PARD3 as a potential preventive target of liver tumorigenesis via TIC regulation.

Indexed as

Adaptor Proteins, Signal TransducingCarcinoma, HepatocellularCell Cycle ProteinsLiver NeoplasmsCarcinogenesisCell Line, TumorCell Transformation, NeoplasticCholineHedgehog ProteinsHumansNeoplastic Stem CellsRNA, Guide, CRISPR-Cas SystemsAdaptor Proteins, Signal TransducingCell Cycle ProteinsCholineHedgehog ProteinsPARD3 protein, humanRNA, Guide, CRISPR-Cas SystemsBerberineCancer stem cellsHepatic tumorigenesisPARD3Sonic hedgehog

Identifiers

PMID38317186
PMCPMC10845773

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Registered trials

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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.