Evidence map›Paper›PMID 26257059›Full record

ArticleOncogene2016

NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial-mesenchymal transition.

H-J Li, P-N Yu, K-Y Huang, H-Y Su, T-H Hsiao, C-P Chang, M-H Yu, Y-W Lin

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  7. Article
  8. Review
  9. Review
  10. Article
  11. Implicating the cholecystokinin B receptor in liver stem cell oncogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  12. Article
  13. Metastasis Inhibition.International journal of molecular sciences · 2023
    Article
  14. Article
  15. The emerging role of ISWI chromatin remodeling complexes in cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
  16. Article
  17. Article
  18. 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

8 authors at 3 institutions in 1 country.

H-J LiGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, Republic of China.
P-N YuDepartment and Graduate Institute of Microbiology and Immunology, National Defense Medical Center, Taipei, Taiwan, Republic of China.
K-Y HuangGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, Republic of China.
H-Y SuDepartment of Obstetrics and Gynecology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China.
T-H HsiaoDepartment of Medical Research, Taichung Veterans General Hospital, Taipei, Taiwan, Republic of China.
C-P ChangDepartment and Graduate Institute of Microbiology and Immunology, National Defense Medical Center, Taipei, Taiwan, Republic of China.
M-H YuDepartment of Obstetrics and Gynecology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China.
Y-W LinGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, Republic of China.
National Defense Medical Center · TWTaichung Veterans General Hospital · TWTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor NKX6.1 (NK6 homeobox 1) is important in the development of pancreatic β-cells and neurons. Although recent publications show that NKX6.1 is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the metastasis suppressor function of human NKX6.1 using cell, animal and clinical analyses. Our data show that NKX6.1 represses tumor formation and metastatic ability both in vitro and in vivo. Mechanistically, NKX6.1 suppresses cell invasion by inhibiting the epithelial-to-mesenchymal transition (EMT). NKX6.1 directly enhances the mRNA level of E-cadherin by recruiting BAF155 coactivator and represses that of vimentin and N-cadherin by recruiting RBBP7 (retinoblastoma binding protein 7) corepressor. Clinical cancer tumors with metastasis show low NKX6.1 protein expression coinciding with low E-cadherin and high vimentin expression. Our results demonstrate that NKX6.1 functions as an EMT suppressor by interacting with different epigenetic modifiers, making it a potential novel therapeutic option.

Indexed as

AnimalsCadherinsCell Line, TumorDNA MethylationEpigenesis, GeneticEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHomeodomain ProteinsHumansMiceNeoplasm InvasivenessRetinoblastoma-Binding Protein 7RNA, MessengerTranscription FactorsVimentinCadherinsHomeodomain ProteinsNKX6-1 protein, humanRBBP7 protein, humanRetinoblastoma-Binding Protein 7RNA, MessengerSMARCC1 protein, humanTranscription FactorsVimentin

Identifiers

PMID26257059
PMCPMC4855079
OpenAlexW1153843643

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.