Evidence map›Paper›PMID 34521817›Full record

ArticleCell death & disease2021

Programmed cell death 10 promotes metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma via PP2Ac-mediated YAP activation.

Bo Sun, Fang-Jing Zhong, Cong Xu, Yi-Ming Li, Yan-Rong Zhao, Mo-Mo Cao, Lian-Yue Yang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  6. PDCD10/CCM3, a potential target for pancreatic ductal adenocarcinoma?Clinical science (London, England : 1979) · 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

7 authors at 1 institution in 1 country.

Bo SunLiver Cancer Laboratory, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.ORCID 0000-0002-7999-7071
Fang-Jing ZhongLiver Cancer Laboratory, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Cong XuLiver Cancer Laboratory, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yi-Ming LiLiver Cancer Laboratory, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yan-Rong ZhaoLiver Cancer Laboratory, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Mo-Mo CaoLiver Cancer Laboratory, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Lian-Yue YangLiver Cancer Laboratory, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. lianyueyang@hotmail.com.ORCID 0000-0002-8805-872X
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour metastasis is the main cause of postoperative tumour recurrence and mortality in patients with hepatocellular carcinoma (HCC), but the underlying mechanism remains unclear. Accumulating evidence has demonstrated that programmed cell death 10 (PDCD10) plays an important role in many biological processes. However, the role of PDCD10 in HCC progression is still elusive. In this study, we aimed to explore the clinical significance and molecular function of PDCD10 in HCC. PDCD10 is significantly upregulated in HCC, which also correlates with aggressive clinicopathological characteristics and predicts poor prognosis of HCC patients after liver resection. High PDCD10 expression promotes HCC cell proliferation, migration, and invasion in vitro and tumour growth, metastasis in vivo. In addition, PDCD10 could facilitate epithelial-to-mesenchymal transition (EMT) of HCC cells. In terms of the mechanism, PDCD10 directly binds to the catalytic subunit of protein phosphatase 2A (PP2Ac) and increases its enzymatic activity, leading to the interaction of YAP and dephosphorylation of the YAP protein. This interaction contributes to YAP nuclear translocation and transcriptional activation. PP2Ac is necessary for PDCD10-mediated HCC progression. Knocking down PP2Ac abolished the tumour-promoting role of PDCD10 in the migration, invasion and EMT of HCC. Moreover, a PP2Ac inhibitor (LB100) could restrict tumour growth and metastasis of HCC with high PDCD10 expression. Collectively, PDCD10 promotes EMT and the progression of HCC by interacting with PP2Ac to promote YAP activation, which provides new insight into the mechanism of cancer metastasis. PDCD10 may be a potential prognostic biomarker and therapeutic target for HCC.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsApoptosis Regulatory ProteinsCarcinoma, HepatocellularCell Line, TumorCell MovementCell NucleusCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMembrane ProteinsMiceApoptosis Regulatory ProteinsMembrane ProteinsPDCD10 protein, humanProtein Phosphatase 2Proto-Oncogene ProteinsRNA, MessengerYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID34521817
PMCPMC8440642
OpenAlexW3201643453

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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.