Evidence map›Paper›PMID 31477838›Full record

ArticleOncogene2020

Cellular prion protein transcriptionally regulated by NFIL3 enhances lung cancer cell lamellipodium formation and migration through JNK signaling.

Shin-Chih Lin, Chia-Hung Lin, Nien-Chu Shih, Hsin-Ling Liu, Wen-Chao Wang, Kun-Yang Lin, Zih-Yu Liu, Yu-Jhen Tseng, Hsueh-Kai Chang, Yi-Cheng Lin and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. CORN 2.0 - Condition Orientated Regulatory Networks 2.0.Computational and structural biotechnology journal · 2025
    Article
  7. Article
  8. Article
  9. Upregulated PrPNPJ precision oncology · 2024
    Article
  10. PrPOncogene · 2024
    Article
  11. Article
  12. The Humanization and Maturation of an Anti-PrPc Antibody.Bioengineering (Basel, Switzerland) · 2024
    Article
  13. Review
  14. Article
  15. Review
  16. Emerging roles of the cellular prion protein (PrPCellular and molecular life sciences : CMLS · 2023
    Review
  17. A new border for circadian rhythm gene NFIL3 in diverse fields of cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  18. Review
  19. The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022
    Review
  20. High Expression ofCancers · 2022
    Article
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

16 authors at 4 institutions in 2 countries.

Shin-Chih Lin *Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei, 11221, Taiwan.
Chia-Hung Lin *Division of Molecular Pathology, Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, 11221, Taiwan.ORCID http://orcid.org/0000-0002-1819-7310
Nien-Chu ShihInstitute of Clinical Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
Hsin-Ling LiuInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, 11221, Taiwan.
Wen-Chao WangInstitute of Clinical Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
Kun-Yang LinInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, 11221, Taiwan.ORCID http://orcid.org/0000-0002-6197-3995
Zih-Yu LiuInstitute of Clinical Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
Yu-Jhen TsengInstitute of Clinical Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
Hsueh-Kai ChangInstitute of Clinical Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
Yi-Cheng LinDivision of Molecular Pathology, Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, 11221, Taiwan.
Yi-Chen YehDivision of Molecular Pathology, Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, 11221, Taiwan.
Hiroshi MinatoDepartment of Pathology and Laboratory Medicine, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa, 920-0293, Japan.
Takeshi FujiiDepartment of Pathology, Toranomon Hospital, 2-2-2 Toranomon, Minato-ku, Tokyo, 105-8470, Japan.ORCID http://orcid.org/0000-0001-7237-1183
Yu-Chung WuDivision of Thoracic Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei, 11221, Taiwan.
Mei-Yu ChenProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei, 11221, Taiwan. meychen@ym.edu.tw.
Teh-Ying ChouProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei, 11221, Taiwan. tychou@vghtpe.gov.tw.
National Yang Ming Chiao Tung University · TWTaipei Veterans General Hospital · TWKanazawa Medical University · JPToranomon Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor invasion and metastasis are the major causes of treatment failure and mortality in lung cancer patients. In this study, we identified a group of genes with differential expression in in situ and invasive lung adenocarcinoma tissues by expression profiling; among these genes we further characterized the association of the upregulation of PRNP, the gene encoding cellular Prion protein (PrPc), with lung adenocarcinoma invasiveness. Immunohistochemistry on clinical specimens showed an association of PrPc expression with invasive but not in situ lung adenocarcinoma. Consistently, the expression of PrPc was higher in the highly invasive than in the lowly invasive lung adenocarcinoma cell lines. Knockdown of PrPc expression in cultured lung adenocarcinoma cells decreased their lamellipodium formation, in vitro migration and invasion, and in vivo experimental lung metastasis. Phosphorylation of JNKs was found to correlate with PrPc expression and the inhibition of JNKs suppressed the PrPc-induced up-regulation of lamellipodium formation, cell migration, and invasion. Moreover, we identified the nuclear factor, interleukin 3 regulated (NFIL3) protein as a transcriptional activator of the PRNP promoter. Accordingly, NFIL3 promoted lung cancer cell migration and invasion in a PrPc-dependent manner. High NFIL3 expression in clinical specimens of lung adenocarcinoma was also associated with tumor invasiveness. Overall, our observations suggest that the NFIL3/PrPc axis, through regulating lamellipodium formation and cell mobility via JNK signaling, plays a critical role in lung cancer invasiveness and metastasis.

Indexed as

AnimalsBasic-Leucine Zipper Transcription FactorsCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansIn Situ HybridizationLung NeoplasmsMaleMAP Kinase Signaling SystemMiceNeoplasm InvasivenessNeoplasm MetastasisOligonucleotide Array Sequence AnalysisPrion ProteinsBasic-Leucine Zipper Transcription FactorsNFIL3 protein, humanPrion ProteinsPRNP protein, human

Identifiers

PMID31477838
OpenAlexW2971977666

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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.