Evidence map›Paper›PMID 31844057›Full record

ArticleNature communications2019

PSPC1-interchanged interactions with PTK6 and β-catenin synergize oncogenic subcellular translocations and tumor progression.

Yaw-Dong Lang, Hsin-Yi Chen, Chun-Ming Ho, Jou-Ho Shih, En-Chi Hsu, Roger Shen, Yu-Ching Lee, Jyun-Wei Chen, Cheng-Yen Wu, Hsi-Wen Yeh and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 40 citations in OpenAlex.

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  10. MCell death & disease · 2025
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  14. Paraspeckle Component 1: a multifunctional RNA binding protein.American journal of cancer research · 2025
    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

12 authors at 4 institutions in 1 country.

Yaw-Dong LangInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.ORCID http://orcid.org/0000-0002-4152-587X
Hsin-Yi ChenGraduate Institute of Cancer Biology & Drug Discovery, College of Medical Science & Technology, Taipei Medical University, Taipei, 11031, Taiwan.
Chun-Ming HoInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.
Jou-Ho ShihInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.
En-Chi HsuInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.ORCID http://orcid.org/0000-0002-5671-6169
Roger ShenInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.
Yu-Ching LeeTMU Research Center of Cancer Translational Medicine, Taipei Medical University, Taipei, 11031, Taiwan.
Jyun-Wei ChenInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.
Cheng-Yen WuInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.
Hsi-Wen YehInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.ORCID http://orcid.org/0000-0001-5535-5245
Ruey-Hwa ChenInstitute of Biological Chemistry, Academia Sinica, Taipei, 11529, Taiwan.ORCID http://orcid.org/0000-0001-8124-5832
Yuh-Shan JouInstitute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan. jou@ibms.sinica.edu.tw.ORCID http://orcid.org/0000-0001-5090-3732
Institute of Biomedical Sciences, Academia Sinica · TWNational Yang Ming Chiao Tung University · TWTaipei Medical University · TWInstitute of Biological Chemistry, Academia Sinica · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide due to metastasis. Paraspeckle component 1 (PSPC1) upregulation has been identified as an HCC pro-metastatic activator associated with poor patient prognosis, but with a lack of targeting strategy. Here, we report that PSPC1, a nuclear substrate of PTK6, sequesters PTK6 in the nucleus and loses its metastasis driving capability. Conversely, PSPC1 upregulation or PSPC1-Y523F mutation promotes epithelial-mesenchymal transition, stemness, and metastasis via cytoplasmic translocation of active PTK6 and nuclear translocation of β-catenin, which interacts with PSPC1 to augment Wnt3a autocrine signaling. The aberrant nucleocytoplasmic shuttling of active PTK6/β-catenin is reversed by expressing the PSPC1 C-terminal interacting domain (PSPC1-CT131), thereby suppressing PSPC1/PTK6/β-catenin-activated metastasis to prolong the survival of HCC orthotopic mice. Thus, PSPC1 is the contextual determinant of the oncogenic switch of PTK6/β-catenin subcellular localizations, and PSPC1-CT131 functions as a dual inhibitor of PSPC1 and PTK6 with potential for improving cancer therapy.

Indexed as

AdultAgedAnimalsbeta CateninCarcinoma, HepatocellularCell Line, TumorCell NucleusCytoplasmDisease ProgressionEpithelial-Mesenchymal TransitionFemaleHumansKaplan-Meier EstimateLiverLiver NeoplasmsMalebeta CateninCTNNB1 protein, humanNeoplasm ProteinsProtein-Tyrosine KinasesPSPC1 protein, humanPTK6 protein, humanRNA-Binding ProteinsWnt3A ProteinWNT3A protein, human

Identifiers

PMID31844057
PMCPMC6914800
OpenAlexW2996096071

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.